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Renal > Renal Physiology II > Flashcards

Renal Physiology II Flashcards

1
Q

Note that constriction of the efferent arteriole will cause

A

Back pressure within the glomerulus

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2
Q

In a healthy nephron, any increase in pressure within the glomerulus will increase

A

GFR

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3
Q

Low resistance and relatively high pressure environment when compared to that of the systemic capillary network

A

Between afferent and efferent ends of glomerulus

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4
Q

The combination of low resistance, high pressure (50 mmHg), and enormous surface area of the glomerulus enables the filtration of approximately

A

180 L of plasma per day

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5
Q

Regulated by the same SNS norepinephrine-adrenoreceptor-dependent mechanism of action that occurs in peripheral vascular smooth muscle

A

Flow within afferent arteriole

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6
Q

Functions via the intricate concerted actions of the SNS, natiuretic peptides, paracrine factors, and the RAAS

A

Autoregulation of afferent arteriole flow

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7
Q

Via autoregulation, a fairly narrow range of GFR and RBF can be maintained even in the face of markedly changing

A

MAP

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8
Q

Occurs in response to 1.) pressure-induced distension of both vascular smooth muscle and the vascular endothelium within the afferent arteriole, and 2.) the tubular glomerular feedback system

A

Autoregulation

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9
Q

Pressure-induced distension of both vascular smooth muscle and the vascular endothelium within the afferent arteriole is essentially just

A

Stress induced activation of cation channels, depolarization, Ca2+ influx, and contraction

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10
Q

Uses feedback between several components of the nephron and its microvasculature

A

Tubular-glomerular-feedback (TGF) system

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11
Q

Regulated by the concentrations of Na+ (or NaCl) in the forming urine as it reaches the cortical thick ascending limb (TAL)

A

TGF System

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12
Q

In this region of the TAL, there is a population of specialized cells collectively known as the

A

Macula Densa

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13
Q

These macula densa cells are in close approximation with the

A

Juxtaglomerular (JG) apparatus

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14
Q

Imbedded around the afferent arteriole

A

JG apparatus

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15
Q

The JG apparatus contains JG cells (modified smooth muscle cells) that secrete

A

Renin

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16
Q

As GFR is increased to the upper physiologic limits, we see

A

Lots of H2O and NaCL in the forming urine

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17
Q

This increased urine NaCl load traverses the nephron to the region of the

A

Macula Densa

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18
Q

At the macula densa, NaCl delivery (a signal for elevated GFR) stimulates the depolarization of

A

Macula ensa cells

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19
Q

Upon activation, these macular cells secrete many factors including ATP, adenosine, and thromboxane, each of which target and promote

A

Vasoconstriction of the afferent arteriole

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20
Q

Vasoconstriction of the afferent arteriole lowers glomerular P, which down-modulates

A

GFR

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21
Q

In the event of exxagerated volume expansion (increased ECF volume), the sensitivity of the TGF mechanism is decreased because the result of increased GFR is a substantial increase in

A

H2O and Na+ filtration (pressure natriuresis)

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22
Q

There is lots of Na+ in the filtrate, but there is a lot more H2O, thus the lumenal [Na+] is relatively

A

Low

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23
Q

Under these conditions, what is the consequence of the relatively low lumenal [Na+]?

A

The TGF mechanism is more or less desensitized

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24
Q

This sustains a higher

A

Glomerular P

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25
Q

The higher glomerular P causes increaed GFR, and therefore promotes a higher volume of urine excretion in order to promote

A

Restoration of BP

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26
Q

In summary, the TGF mechanism is an acute regulator of

A

GFR

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27
Q

By using Na+ in forming urine as a marker of GFR, the TGF system indirectly interprets volume-pressure status using glomerular pressure and filtration and modulates GFR by controlling

A

Afferent smooth muscle tone

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28
Q

What are the most important hormones for regulation of renal function?

A

The members of the RAS, arginine vasopressin (ADH or vasopressin), atrial natriuretic peptide (ANP), norepinephrine, and aldosterone

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29
Q

The only one of these hormones that does not have a direct role in the control of GFR and RBF (renal blood flow) is

A

Aldosterone

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30
Q

A key component of renal function, and this begins with the mediation of renal organogenesis in utero

A

Renin-Angiotensin System (RAS)

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31
Q

Throughout life, the RAS functions via endocrine, paracrine, and autocrine mechanisms to modulate

A

Renal BP and thus regulate GFR

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32
Q

Renal Na+ reabsorption is also modulated by

A

An-II

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33
Q

A potent vasoconstrictor

A

An-II

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34
Q

The relatively inert precursor hormones of An-II are

A

Angiotensinogen and An-I

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35
Q

All components of the RAS are expressed in the

A

Kidney

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36
Q

Expressed within proximal tubule cells

A

Angiotensinogen

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37
Q

Present within the proximal tubule brush border

A

Angiotensin converting enzyme (ACE)

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38
Q

There is also an extrarenal RAS system. This system still depends upon renin from JG secretionm but the angiotensinogen is produced and secreted by

A

Hepatocytes

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39
Q

Expressed in renal and cardiac tissues where it converts An-II into angiotensin 1-7

A

ACE2

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40
Q

angiotensin 1-7 binds to Mas, a G-protein coupled receptor, to stimulate

A

Vasodilation, block proliferation, and promote bradykinin production

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41
Q

Angiotensin 1-7 has actions which counter those of

A

An-II

42
Q

Angiotensinogen is targeted by

A

Renin

43
Q

A protein hormone that is produced and secreted by the JG cells

A

Renin

44
Q

Renin secretion is regulated by which 5 things?

A
  1. ) SNS tone (JG cells have B1 adrenoreceptors)
  2. ) Distension of afferent arteriolar endothelium (elevated BP)
  3. ) Signals from macula densa
  4. ) ANP
  5. ) Negative feedback by An-II
45
Q

Renin catalyzes the conversion of angiotensinogen into

A

An-I

46
Q

The conversion of angiotensinogen into the An-I is the basis for the

-An indicator of RAS activity

A

Plasma Renin Activity (PRA) assay

47
Q

Volume depletion leads to lowered BP. This would cause secretion of Renin with asubsequent increase in

A

PRA

48
Q

Volume increase leads to elevated BP and the shut off of the

A

RAS (decreased PRA)

49
Q

Catalyzes the conversion of An-I to An-II and also the degredation of bradykinin into inactive peptide fragments

A

Angiotensin Converting Enzyme (ACE)

50
Q

Bradykinin functions as a

A

Vasodilator

51
Q

This, ACE supports vasoconstriction in which two ways?

A
  1. ) Production of An-II

2. ) Degredation of bradykinin

52
Q

During periods of hypovolemia such that normal perfusion pressure can not be maintained, signals are sent to mobilize the

A

RAS

53
Q

An-II induces vasoconstriction of systemic arterioles. This raises

A

BP

54
Q

An-II dependent constriction of the efferent arteriole steadies

A

Glomerular P

55
Q

With constriction of the efferent arterioles by An-II, renal perfusion is reduced leading to lowered P within the

A

Peritubular capillaries

56
Q

This enables increased reabsorption of

A

Na+ and H2O

57
Q

An-II binds two members of the seven transmembrane G-protein-coupled receptor family known as

A

AT1 and AT2

58
Q

Expressed within the smooth muscle of afferent and predominantly efferent arterioles, renal tubules, and peripheral vasculature

-Predominant AT receptor expressed in humans

A

AT1

59
Q

In the event of diminished ECV, An-II binds and activates AT1 within the

A

Efferent arteriole vascular smooth muscle

60
Q

This induces efferent vasoconstriction and maintains glomerular pressure in order to sustain optimal ultrafiltration across the

A

Glomerular capillaries

61
Q

AT1 is also expressed within renal tubules and cells within the

A

Adrenal zona glomerulosa

62
Q

Studies in mice have shown that AT1 activity is coupled to the activation of the transporters NHE3, NKCC, NCC, and ENaC, all of which enable

A

Na+ reabsorption

63
Q

The main stimulus for aldosterone production and secretion in the adrenal cortex

A

An-II

64
Q

AT1 is regionally expressed within the

A

Renal tubule epithelium and JG cells

65
Q

Has the ability to both up and down regulate the RAS

A

An-II

66
Q

Known to mediate An-II dependent vasoconstriction in the renal efferent arterioles and An-II stimulated Na+ reabsorption from the tubules

A

AT1

67
Q

Represents a multileveled feedback-dependent control mechanism for mediating

A

GFR and Na+ reabsorption

68
Q

What are three pharmalogical mechanisms designed to target the RAS

A
  1. ) ACE inhibitors (enalapril)
  2. ) ARBs (losartan)
  3. ) Renin inhibitors (aliskiren)
69
Q

Has been localized to lung, renal coronary, myocardial tissues, as well as cardiac fibroblasts in the adult

-prevalent during fetal organogenesis

A

AT2

70
Q

Experimental evidence indicates that AT2 mediates

A

Vasodilation and natriuresis

71
Q

Within renal vascular smooth muscle, promotes the nitric oxide synthase-mediated production of nitric oxide, activation of guanylyl cyclase, the subsequent generation of cGMP

A

AT2

72
Q

The nitric oxide synthase-mediated production of nitric oxide, activation of guanylyl cyclase, and the subsequent generation of cGMP is a signaling motif that promotes

A

Vasodilation

73
Q

The activation of AT2 can also induce

A

Bradykinin secretion (a vasodilator and natriuretic factor)

74
Q

Therefore, the effectos of an ARB may be multi-tierd by

A
  1. ) Direct block of AT1 mediated vasoconstriction and Na+ reabsorption
  2. ) Promoting AT2 release of bradykinin
  3. ) Promoting AT2 dependent vasodilation and natriuresis
75
Q

A renin inhibitor that binds with high specificity to the proteolytic active sites within renin and thus blocks its activity

A

Aliskiren

76
Q

If renin and/or ACE is blocked, then we disrupt the production of

A

An-II

77
Q

Thus, renin and ACE inhibitors can allevite which effects of An-II

A

An-II’s vasoconstrictive and antinatriuretic effects

78
Q

In addition, an ACE inhibitor will prevent the ACE-dependent degradation of

A

Bradykinin

79
Q

Renin and ACE inhibitors will also tend to lower levels of which hormone?

A

Aldosterone

80
Q

However, there are ACE independent pathways for synthesis of

A

An-II

-ACE independent pathways account for 40% of intrarenal An-II

81
Q

Also, when An-Ii production is impaired, we actually lose the short loop feedback inhibition of renin. Thus,

A

Renin activity (measured as PRA) actually increases

82
Q

This phenomenon is referred to as the

A

ACE escape

83
Q

PREganglionic SNS fibers innervate the

A

Adventitia of renal arteries, tubules, and JG apparatus

84
Q

POSTganglionic SNS fibers secrete

A

Norepinephrine

85
Q

Targets both the afferent and efferent arterioles

A

Norepinephrine

86
Q

Activates post-junctional a1 adrenoreceptors within vascular smooth muscle

A

Norepinephrine

87
Q

The resulting vasoconstrictive action induces a collective reduction in

-maintains plasma volume

A

GFR and renal perfusion

88
Q

Norepinephrine also stimulates renin secretion from JG cells by binding

A

B1 adrenoreceptors

89
Q

Elevated SNS activity can enhance some degree of H2O and Na+ reabsorption from tubules via

A

a2 adrenoreceptors

90
Q

Thus the collective pattern of increased SNS activity is the

A

Production of An-II,m conservation of plasma volume by slowing GFR, and enhancing Na+ and H2O reabsorption

91
Q

A protein hormone that is secreted by neurons that terminate within the posterior pituitary

A

Arginine Vasopressin (AVP, aka ADH or vasopressin)

92
Q

AVP is the neuroendocrine hormone that induces the renal-dependent conservation of plasma volume by stimulating

A

H2O and Na+ reabsorption

93
Q

AVP also functions as a

A

Vasoconstrictor

94
Q

In response to hypoosmolality, osmoreceptors within the neurons of the organus, vasculosus lamina terminales are

A

Activated

95
Q

Activation of these osmoreceptors initiates a signal that causes the nerve termini within the posterior pituitary to secrete

A

AVP

96
Q

AVP stimulates vasoconstriction within the renal microcirculation and peripheral arterioles by binding to the

A

V1a receptor isoform

97
Q

Within the nephron, AVP binds the V2 receptor isoform where it promotes

A

H2O reabsorption.

98
Q

AVP promotes H2O reabsorption by inducing the expression and activation of

A

Aquaporin protein-2 (AQP2)

99
Q

Also increases the rate of active Na+ reabsorption from the TAL and DCT via its effects on NKCC (TAL), NCC (DCT), and the tubule epithelial Na+ channel (ENaC) (DCT)

A

AVP

100
Q

The third isoform of AVP receptor that is expressed in the anterior pituitary, and activation of this receptor is coupled to the secretion of adrenocorticotropic hormone (ACTH)

A

V1b

Renal (10 decks)

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