Sweep 1 Flashcards
1
Q
LDLs in the circulation are endocytosed into the
A
steroidogenic cell and lysed to produce cholesterol esters which have low solubility in water, and can be stored in lipid droplets
2
Q
. Steroidogenic cells store cholesterol esters so typically the cells will appear
A
white or fatty
3
Q
Steroid Synthesis usually stimulated by
A
peptide hormones from other glands –
4
Q
activate a G protein coupled receptor →
Steroidogenesis
A
activate adenyl cyclase → increase cAMP → activate PKA which stimulates activity of cholesterol esterases → release cholesterol from intracellular stores
5
Q
Anterior pituitary –
A
adenohypophysis
6
Q
Posterior pituitary =
A
neurohypophysis
7
Q
hypothalamic hormones are transported in the blood within the ————- to the anterior pituitary
A
portal vessels
8
Q
In the anterior pituitary are
A
5 different cell types that produce 6 primary hormones in response to different hypophysiotropic hormones (that were secreted by hypothalamic neurons)
9
Q
CRH—->
A
stimulates ACTH secretion
10
Q
Thyrotropin releasing hormone TRH —->
A
stimulates secretion of TSH
11
Q
GHRH—>
A
stimulates GH secretion
12
Q
Somatostatin SS—>
A
inhibits GH secretion
13
Q
GnRH - gonadotropin releasing hormone—->
A
stimulates secretion of LH and FSH
14
Q
Dopamine—>
A
Inhibitis prolactin
15
Q
POMC is a
A
precursor polypeptide synthesized in corticotrophs that is cleaved to yield multiple peptides with varied actions and target tissues. Products: β - lipotropin and β- endorphin
16
Q
Secretion of thyroid hormones is stimulated by
A
TSH (thyroid stimulating hormone) which is released from the anterior pituitary in response to TRH (thyrotropin releasing hormone) from the hypothalamus.
17
Q
TSH receptors are on the
A
follicle cells;
18
Q
TSH also acts to increase the
A
synthetic activity of the follicle cells and stimulates hyperplasia (and replication). Stimulation of endocytosis of colloid back into follicle cell.
19
Q
TSH also acts to increase the
A
synthetic activity of the follicle cells and stimulates hyperplasia (and replication). Stimulation of endocytosis of colloid back into follicle cell.
20
Q
TH can lead to
A
upregulation of β-adrenergic receptors that are critical for responses to activation of the sympathetic nervous system; increases sensitivities to catecholamines in both the endocrine and nervous systems (vasoconstriction and contraction of cardiac muscle; critical for sympathetic stimulation), also acts on the lungs and smooth muscle
regulates production of growth hormone (GH)- synthesis and interacts with effects of GH in bone; formation of skeletal bone
21
Q
Thyroid Disorders are due to under- or overproduction of TH because of
A
disruption of the feedback mechanism that normally controls TH synthesis and secretion.
22
Q
Without iodine, there is insufficient production of TH → lack of negative feedback increases
A
TRH and TSH secretion → growth of a goiter in response to TH stimulations
23
Q
• The symptoms of moderate hypothyroidism are due to the effects of reduced
A
β-adrenergic receptors, and the disruption of responses to catecholaminergic stimulation
24
Q
Graves disease is an autoimmune disease that is a common cause of hyperthyroidism. Antibodies are produced against
A
TSH, and these antibodies are able to activate the TSH receptor so there is no feedback regulation of thyroid function.
25
In graves disease, TH concentrations are
• TH concentrations are high even though TSH (and TRH) are low due to the feedback effects of increased TH.
26
Secondary defects causing hyperthyroidism include tumors that secrete
TSH without responding to feedback control by TH.
27
• Several antithyroid drugs act to inhibit iodination of
TYR, block the release of TH, or ameliorate the effects of TH in peripheral tissues. Can block T3 peripherally.
28
Adrenal medulla: Most of what is secreted is
epinephrine (E
29
Norepinephrine (NE) is secreted by other postganglionic neurons in the SNS, but the adrenal medulla contains significant amounts of
the enzyme phenyl-N-methyltransferase which converts NE to E.
30
There is also an effect of E and NE on organs and tssues not directly innervated by postganglionic neurons including the liver, skeletal muscle, and fat. In these tissues, epinephrine acts to increase the availability of
metabolic fuel by stimulating lipolysis, glycogenolysis and gluconeogenesis.
31
the cells in the zona glomerulosa contain high levels of
aldosterone synthase, and are deficient in the enzymes that convert corticosterone to cortisol or androgens.
32
The principle action of aldosterone is to stimulate
Na+ and H2O retention by the kidney in order to maintain blood volume and blood pressure.
33
The mechanisms by which aldosterone helps reabsorb Na+ and H2O in the kidney results in an increase in urinary excretion of
K+ and H+.
34
The aldosterone-receptor complex binds to DNA and stimulates the
synthesis of proteins that act to increase Na+ and H2O reabsorption from the tubular fluid back into the blood.
35
Aldosterone can lead to increased synthesis of
mitochondrial enzymes used in oxidative phosphorylation (electron transport system)
36
The secretion of aldosterone is regulated by multiple factors (ACTH has a minor/negligible effect).
* stimulated by an increase in plasma angiotensin II – angiotensin II is a hormone produced in response to renin, a hormone released by the kidney in response to a decrease in Na+ or blood pressure.
* stimulated by an increase in plasma K+ -
* stimulated by a decrease in plasma pH or increase in plamsa H+ -
* stimulated by a drop in systemic blood pressure –
* inhibited by increased Na+ intake –
37
Glucocorticoids, cortisol and corticosterone, are secreted by the cells of the .
zona fasciculata
38
Glucocorticoids, cortisol and corticosterone:
• ↓ immune and inflammatory responses- inhibits cytokine production.
39
Glucocorticoids, cortisol and corticosterone: • permissive action on β-adrenergic receptors in vascular smooth muscle to regulate
blood pressure. Increases receptor expression*
40
Cortisol has a negative feedback action on both
CRH and ACTH.
41
Sex steroids (mostly androgens) are secreted by the
zona reticularis;
42
androstenedione is synthesized by enzymatic conversion of
DHEA
43
in females, E2 has positive feedback actions on
LH secretion prior to ovulation.
44
11. Gigantism is caused by a pituitary tumor that inhibits feedback regulation and leads to a prepubertal onset of excess GH.
T or F
F
45
10. This hormone stimulates prepubertal bone growth.
a) Testosterone
b) Estradiol
c) Progesterone
d) hCG
b
46
9. Which endocrine defect is due a mutation in steroidogenic enzymes that presents with increased adrenal androgen syndrome. Genotype XX with a predominantly male phenotype.
a) Congenital adrenal hyperplasia
b) 5〈 reductase deficiency
c) Androgen insensitivity
a
47
8. During the uterine cycle, ________ from developing follicles stimulates endometrial proliferation.
a) FSH
b) LH
c) Estrogen
d) Progesterone
c
48
7. During the ovarian cycle, there are increased levels of FSH and LH during follicular development. A subsequent decrease in FSH causes the dominant follicle to trigger release of increased estradiol and inhibin.
a) Both statements are true
b) First true second false
c) First false second true
d) Both statements are false
a
49
6. This hormone increases mitosis in follicles, regulates oocyte development, leads to the development of secondary sex characteristics, regulates bone deposition as well as mood.
a) Estradiol
b) Progesterone
c) Testosterone
d) DHEA
a
50
1. Which cells are located in the lining of the ovarian follicle and convert androstenedione to estradiol as well as secreting inhibin in response to FSH?
a) Follicular cells
b) Theca cells
c) Cumulus oophorus
d) Granulosa cells
b
51
3. This disease affects the adrenal glands. It is usually due to a pituitary tumor that leads to excess catabolism and presents with diabetes-like symptoms.
a) Addison’s disease
b) Cushing’s syndrome
c) Crohn’s disease
d) Asthma
b
52
2. There are two principle androgens secreted by the adrenal gland. Which one is more potent and is the main extragonadal source of testosterone and estradiol?
a) DHEA
b) Androstenedione
b
53
2. Leydig cells or interstitial cells lie outside of the
seminiferous tubules.
54
Leydig cells synthesize
T in response to LH.
55
In the gonad, T regulates
spermatogenesis.
56
3. Sertoli cells or sustentacular cells are the
epithelial cells lining the seminiferous tubules.
57
In response to FSH, sertoli cells regulate
spermatogenesis and produce the peptide hormone inhibin.
58
Sertoli cells: Inhibin has negative feedback actions on
FSH secretion.
59
aromatase: T → -------- OR androstenedione → --------- by aromatase in brain and bone
estradiol, estrone
60
There are four types of cells in the ovary with important reproductive functions.
oocyte, theca, granulosa, luteal
61
Shortly after birth, all oocytes are arrested in
prophase of meiosis I.
62
2. Theca cells surround each
follicle; location and function is analogous to that of Leydig cells.
63
Theca cells =
leydig cells
64
3. Granulosa cells are the
epithelial cells of the follicle (analogous to Sertoli cells).
65
In an early follicle, one or more layers of granulosa cells surround the
oocyte. Large, developing follicles become filled with fluid, and some granulosa cells continue to surround the oocyte in the cumulus oophorus.
66
Granulosa cells =
sertoili cells
67
4. Luteal cells are present after ovulation when the
theca and granulosa cells from the ovulatory follicle are transformed into the cells of the corpus luteum.
68
Theca cells synthesize androstenedione in response to
LH
69
androstenedione diffuses into
granulosa cells
70
In response to FSH, granulosa cells
convert androstenedione to estrone which is converted to estradiol (E2)
71
estradiol: stimulates
granulosa cell function and replication
72
estradiol: regulates
oocyte development
73
estradiol: regulates
female secondary sex characteristics
74
estradiol: important regulator of
bone turnover and arterial function
75
estradiol: typically inhibits
GnRH and LH secretion
76
granulosa cells in response to FSH: secrete
inhibin that has a negative feedback effect on FSH secretion
77
proliferative phase: follicular E2 stimulates
proliferation of the endometrium
78
luteal phase: P and E2 stimulate
uterine secretory activity; increase glandular production of glycogen, increase angiogenesis, decrease contractility
79
Menopause consequences:
gonadotropin and inhibin secretion very high
increase reliance on adrenal steroids
80
Male:
genital tubercle →
urogenital fold →>
labioscrotal folds →
glans of penis
urethra and surrounding penis
scrotum and skin of penis
81
Female
genital tubercle →
urogenital fold →
labioscrotal fold →
glans of clitoris
labia minor and urethral opening
labia majora
82
Congenital adrenal hyperplasia
| adrenal enzyme deficiency results in excess production of
adrenal androgens
caused by more than one mutation and severity varies depending on mutation
83
Congenital adrenal hyperplasia genotype is
XX; phenotype is virilized or more male than female depending on severity
84
Congenital adrenal hyperplasia genotype is
XX; phenotype is virilized or more male than female depending on severity
85
Pregnancy
| There is a dramatic increase in circulating concentrations of steroid hormones during pregnancy due to
placental production
86
CL regresses after ~ 3 months and hCG supports
luteal steroidogenesis
87
placental E2 stimulates
growth of myometrium
88
placental P reduces
uterine contractility and stimulates vasodilation
89
The hormones of the growth axis ------ control growth by their actions in
(GHRH → GH → IGF-1), somatic tissue and the liver.
90
. IGF-1 is necessary for
fetal growth;
91
GH becomes
important later in development.
92
Achondroplasia is reduced growth due to constituitive activation of the
fibroblast growth factor receptor.
93
FGF normally inhibits or regulates
bone growth, and continued activation of its receptor results in abnormally impaired development of cartilage.
94
GH insensitivity or dwarfism is due to the absence of a functional
GH receptor. These individuals do not suffer from diabetes or cancer, but are often obese.
95
GH insensitivity The condition can be treated with
exogenous IGF-1.
96
There are no known defects in
IGF-1 synthesis or for the IGF-1 receptor
97
Malnutrition impairs IGF-1 synthesis independent
of GH
98
GH stimulates
maturation of chondroblasts
99
IGF-1 stimulates
cell division
100
Somatic growth is the result of interactions between
GH and IGF-1
101
GHRH elevated during
sleep
102
SS elevated during the
day
103
IGF-1 and GH inhibit
GH and GHRH secretion, but stimulate SS secretion
104
GH is a
| GH acts in
mitogen – will stimulate cell division.
| opposition to insulin
105
Thyroid hormone is required for synthesis of
GH and manifestation of GH effects.
106
Growth is also controlled by
glucose-regulating hormones.
107
Glucocorticoids inhibit
GHRH secretion.
108
Insulin has actions that oppose
GH and IGF-1
109
At puberty, the epiphyseal plates ossify due to the actions of
E2
110
This can alter the resistance and thereby flow
blood viscosity
111
Flow =
volume per unit time
112
F=
ΔP/R
113
Parasymp:
atria- slows, muscarinic receptors
114
Symp
beta andronergic receptors, atria and ventricles - fast.
115
Bundle of His depolarizes slower than
AV node.
116
The action potential of a myocardial ventricular cell.
The prolonged “plateau” of
depolarization is due to the
```
The prolonged “plateau” of
depolarization is due to the slow
but prolonged opening of
voltage-gated calcium channels
PLUS
closure of potassium channels
```
117
Calcium influx doesn’t allow for
myocardial ventricular cell
repolarizing. Longer refractory period.
118
The action potential of an autorhythmic cardiac cell (nodal):
Sodium ions “leaking” in through
the
```
F-type [funny] channels
PLUS
calcium ions moving in through
the T [calcium] channels cause a
threshold graded depolarization.
```
119
The action potential of an autorhythmic cardiac cell (nodal).
Reopening of
```
potassium channels
PLUS
closing of calcium channels
are responsible for the
repolarization phase.
```
120
if you lose SA node, you get
diff pacemaker, but not in sinus rhythm.
121
Gap junctions lead
SA signal onward - cardiac impulses travel through these
122
Funny channels remove
true resting potential
123
ECG: P wave
atria depolarization
124
ECG: QRS
QRS complex - ventricular depolarization
125
ECG: T wave
Ventricular repolarization
126
ECG can be used to look at
arrhythmias
127
Some people have a potentially lethal defect of ventricular muscle, in which the current through voltage-gated K+ channels is delayed and reduced. How could this defect be detected on their ECG recordings?
t wave is extended
128
How does the electrical signal transfer to contractile force?
ec coupling
129
EC coupling:
calcium enters, leads to release of more calcium (calcium binds to ryanadine receptors which releases calcium). Binds during plateau phase.
This is calcium induced calcium release.
130
Calcium that enters during plateau phase in CICR
is trigger calcium
131
Ventricular cells have
long refractory period to ensure that they can fill.
132
The prolonged refractory period of cardiac muscle
| prevents
tetanus, and allows time for ventricles to
| fill with blood prior to pumping.
133
Stenotic valve
narrowed - there is a murmer
134
Insufficient valve
backflow - it cannot completely close.
135
Wiggers Diagram
top is pressure, middle is volume
136
Aortic, left atrial, left ventricular pressure
wigger's diagram - top to bottom
137
isovolumetric relaxing/contracting
rising pressure and dropping pressure of left ventricular pressure.
138
Right heart and left heart is the same except for
pressure generated.
139
Parasymp only decreases
HR by closing funny channels.
140
Autonomics work
in concert - reduce one, raise other.
141
Preload –
the volume of blood in the ventricles just before contraction. End-diastolic volume
142
Afterload –
the pressure against which the ventricle pumps
143
Symp input into venticle -
beta. Increases contraction, increases stroke volume.
144
Symp increases
calcium availabiility - thus how it contracts harder and faster.
145
High compliance
little change in pressure with more volume. Why veins don't change.
146
Pulse pressure =
```
SP – DP
Determined by:
stoke volume
Speed of ejection of the stroke volume
Arterial compliance
```
147
Compliance =
Δ volume/Δ pressure
148
Mean arterial pressure =
DP + 1/3(SP-DP), CO*TPR
149
Hypertrophic cardiomyopathy particularly in
IV septum
150
Hypertrophic cardiomyopathy is
pre load dependent.
151
Intrinsic tone
| Controlled by:
Local controls - two organs - heart and brain
| Extrinsic controls- everything else
152
Local control - active hyperemia
active hyperemia - changes in metabolites, dilate arterioles.
* Increase in metabolic activity sparks this
* * accumulation of: CO2, H+, K+, eicosanoids, adenosine, bradykinin, nitric oxide (NO)
Also happens with working skeletal muscle
153
Local control - flow autoregulation
* decrease in arterial pressure sparks this. Occurs in every organ
154
Flow autoregulation ** myogenic responses –
some arteriolar smooth muscle respond to increased stretch caused by increased pressure by contracting to a greater extent (Converse is also true).
155
- Reactive hyperemia – response to
cessation of blood flow
156
Endothelial cell monolayer
lining, release paracrine agents for smooth muscle.
157
Sympathetic stimulation of alpha-adrenergic receptors causes
vasoconstriction to decrease blood flow to that location.
158
▪ Sympathetic stimulation of beta-adrenergic receptors leads to
vasodilation to cause an increase in blood flow to that location
159
Local controls will involv
alpha andrenergic receptors
160
Extrinsic controls:
```
Sympathetic nerves
Parasympathetic nerves
Noncholinergic, Nonadrenergic Autonomic neurons (release NO – enteric and penile)
Hormones
Epinephrine
Norepinephrine
Angiotension II
Vasopressin
Atrial natriuretic peptide
```
161
Heart blood vessels
intrinsicl, local.
162
Skeletal
restinjg == symp.
| Active = local
163
Gi tract
all symp. Splanchnic organs. Do have autoregulation, but all extrinsic.
164
Kidney
Extrinsic symp
165
Brain
local
166
Skinb
symp
167
lungs
symp - little control. Gravitational mainly.
168
Paracrine effect
parasymp - regulator in penile blood flow.
169
Endothelium derived relaxing factor (EDRF) =
Nitric oxide (NO) viagra.
170
How can symp lead to vasodilation?
turn it off.
171
More area
less velocity.
172
Low molecular weight penetrating solutes =
crytalloids
173
Non-penetrating plasma proteins =
colloids
174
PC=
capillary hydrostatic pressure (favoring fluid movement out of the capillary
175
PIF=
Interstitial hydrostatic pressure (favoring fluid movement into the capillary)
176
πC=
Osmotic force due to plasma protein concentration (favoring movement into the capillary)
177
πIF=
Osmotic force due to interstitial fluid protein concentration (favoring movement out of the capillary)
178
Net filtration pressure =
PC + πIF - PIF - πC
179
If an accident victim loses 1 L of blood, why would an intravenous injection of a liter of plasma be more effective for replacing the lost volume that injecting a liter of an equally concentrated crystalloid solution? –
increase piC
180
. Sympathetically mediated venoconstriction can substantially
increase venous return to the heart. - Alpha receptors
181
Alterations in “venous return” alter
end-diastolic volume (EDV); and stroke volume, cardiac output.
182
Serum =
plasma with fibrinogen and
| clotting proteins removed
183
Ferritin serves as a
storage buffer for iron
184
Bilirubin –
major breakdown product of hemoglobin
185
Iron released from destroyed RBC is bound by
transferrin and delivered to bone marrow.
186
Folic acid – needed for thymine --> if deficient leads to
impaired cell division
187
B12 – required for action of
folic acid.
188
B12 absorption requires
intrinsic factor.
189
If no intrinsic factor --->
pernicious anemi
190
Erythropoiesis is
| hormonally regulated: decreased oxygen delivery to the kidney causes the secretion of
erythropoietin, which activates receptors in bone marrow, leading to an increase in the rate of erythropoiesis.
191
Hemostasis – the stoppage of bleeding
| Accomplished by 2 processes that occur in rapid succession:
Formation of a platelet plug
Blood coagulation (clotting)
Platelets are critical to both.
192
Blood coagulation (clotting) is the transformation of blood into a solid gel called a clot or thrombus and consist mainly of a protein polymer –
fibrin
193
Thrombin leads to
Platelet activation
194
the extrinsic pathway is the more important of the two under most circumstances for
clotting
195
Coumadin (Warfarin) –
| Blocks
Vitamin K metabolism
196
Moreover, bile salts from the liver facilitate the absorption of
lipids in the diet, including vitamin K,
197
vitamin K,
| which is required for the synthesis of .
prothrombin
198
Vit. K dependent factors =
Coagulation proteins: factors II (prothrombin), VII, IX and X
199
Anticoagulation proteins:
proteins C and S
These proteins have in common the requirement to be post-translationally modified by carboxylation of glutamic acid residues (forming gamma-carboxyglutamic acid) in order to become biologically active.
200
proteins C and S
| These proteins have in common the requirement to be
post-translationally modified by carboxylation of glutamic acid residues (forming gamma-carboxyglutamic acid) in order to become biologically active.
ANTICOAGULATION PROTEINS
201
Following tissue repair, fibrin clots are dissolved in a
| process mediated by
plasmin;
202
synthetic plasminogen
activators can be used immediately after a stroke or
heart attack to help
dissolve clots and restore blood flow
203
The effect of norepinephrine on β1-receptors located on ventricular muscle cells is to
increase the amount of cytosolic (free) Ca2+ and to produce a stronger contraction and an increase in stroke volume.
204
Thus, when the INCREASE in stroke volume is produced by an increase in free Ca2+ , we say that the
CONTRACTILITY of the ventricle is increased.
| This happens during exercise.
205
Therefore, deltaP, which is called the
perfusion pressure, is the same for all vascular beds;
206
delta p =
| perfusion pressure
MAP–VP, where MAP is the mean arterial pressure and VP is the venous pressure.
207
What will the coronary vascular bed have to do if the heart muscle needs more blood flow? (Assume the MAP and the VP to be constant.)
Answer:
Since F = (MAP – VP) / R, it will have to decrease its resistance.
F = deltaP/R ********
208
MAP=
CO*TPR
209
Dynamic changes in vasodilation/vasoconstriction due to changes in the resistance of arterioles can alter the
MAP
210
Compensatory changes in arteriolar resistance occur to protect the
maintenance of mean arterial pressure
211
Mean systemic arterial pressure
F = delta P/R
Delta P = F x R
Systemic vascular system is a series of tube….therefore delta P = mean systemic artereial pressure (MAP) – pressure in the right atrium. F = CO and R = TPR
MAP- Right atrial pressure = CO x TPR
RAP ~O mmHg…… therefore
MAP = CO x TPR
212
Baroreceptor neurons deliver MAP information to the
medulla oblongata’s cardiovascular control center (CVCC);
| the CVCC determines autonomic output to the heart.
213
Increase in baroreceptor firing leads to
increase in psymp, decrease in symp to heart.
214
Other causes of hypotension
Allergic response
Histamine release --> vasodilation
Emotional stress
↓Sympathetic and ↑Parasympathetic
--> vasovagal syncope
215
Increase in CO during exercise
| is due to large increase in
HR and
| smaller increase in SV.
216
VO2max could be limited by:
1- cardiac output
2- respiratory system’s ability to deliver oxygen
3- exercising muscle’s ability to use oxygen
217
Except for highly trained athletes – ------- is the factor that
determines VO2max
CO
218
Hypertension.
| results from
increase in cardiac output or total peripheral resistance
219
Renal hypertension -->
increased renin release -->
| increased angiotension II release (this will lead to increased aldosterone release.)
220
beta andrenergic blockers
decrease CO
221
angiotensin II is a
vasoconstrictor
222
Diastolic dysfunction –
reduced ventricular compliance results in an
increase end-diastolic pressure and thus a decreased end-diastolic
volume and a decreased stroke volume.
223
Systolic dysfunction – a decrease in
cardiac contractility – a lower
| Stroke volume at any given end-diastolic volume.
224
It is not possible, under normal circumstances, to increase one
but not the other of these determinants of cardiac output.
**referringt o HR and stroke volume SV
225
Heart failure leads to increased
fluid retention, leading to
increased blood volume and greater stroke volume;
however, the failing heart is less able to handle a large EDV
226
Sudden cardiac death occurs from
ventricular fibrillation.
227
Thrombolytic therapy
Streptokinase
| tissue plasminogen activator
228
Percutaneous coronary intervention
Balloon angioplasty
| Stenting
229
Repolarization of SA nodal cells occurs via:
```
A) Opening of Ca channels
B) Opening of Na channels
C) Opening of K channels
D) Closing of K channels
E) Na/K ATPase
```
c
230
Funny channels are
sodium channels
231
The length-tension relationship of cardiac muscle is responsible for the
Frank-Starling mechanism.
232
Frank-Starling mechanism matches
the CO to the VENOUS RETURN
| and it matches the outputs of the two VENTRICLES
233
That’s what happens during exercise. The End-diastolic size of the heart doesn’t change and the SV
increases because of sympathetic stimulation.
234
The effect of epinephrine (from the adrenal medulla) or norepinephrine (released by sympathetic fibers) on 1-receptors in heart muscle produces an increase in
contractility
235
Increased adenosine in a metabolically controlled organ will cause:
```
A) vasodilation
B) vasoconstriction
C) decreased blood flow
D) increase diffusion
E) nothing
```
a - it is a metabolite, local controls kick in - active hyperemia.
