exam 1 lecture 7 Flashcards
hyperemia
oxygen deficiency, vasodilation, carbon dioxide, hydogen ions, lactic acid account for
active hyperemia
skeletal muscle, heart and cerebral and splanchnic circulations, blood flow increases with increases metabolic activity. Because of accumulation of vasodilators coupled with initial reduce oxygen tension and nutrient supply
reactive hyperemia
when blood supply to tissue is clamped and then restored, flow through tissue increase by as much as five fold times, accumulation of vasodilators, reduced oxygen tension and depletion of nutrients (BUT can also lead to hypoxic pulmonary vasoconstriction)
autoregulation
when tissues maintain a fairly constant blood flow over a perfusion pressures ranging from 70-175 mmHg. Manly in renal, cerebral and coronary circuits
explanations for autoregulation
flushing vasodilators metabolites out of tissue when flow increases causes vasoconstriction and increase in R, myogenic mechanism: bayliss hypothesis, sudden stretch of the vessels walls provoke arterial and arteriolar smooth muscle to contract, causing vasoconstriction-> decrease flow
fast myogenic response is 50% responsible for renal blood flow autoregulation how?
Tubuloglomerular feedback (NaCl, macula densa, extraglomerular mesangial cells and afferent arterioles) complements the myogenic response.
vasoconstrictors
THE CATECHOLAMINES: Norepinephrine and epinephrine bind β1 adrenergic receptors in the heart,, alpha1 adrenergic receptors in the smooth muscle cells of the media of most blood vessels.Low E concentrations= vasodilator (beta 2)
high E concentrations= vasoconstrictor (alpha 1)
Dopamine
vasoconstrictor: Vasodilator at low concentrations (dopamine receptors), vasoconstrictor at high concentrations
(alpha1 adrenergic receptors). Acts on the heart at moderate doses (β1 adrenergic receptors )
dobutamine
sysnthetic catcholamine primarily with beta 1 activity, inotropic support in cardiogenic shock
Angiotensin II
Octapeptide, amount in the circulation controlled
by renin secreted by the JG cells
Low concentrations= Constricts the renal arteries and stimulates adrenal cortex to secrete aldosterone
High concentrations: Generalized vasoconstriction
angiotensin II blockers
ACE inhibitors used for anti-hypertensive therapies
ADH, or vasopressin
increased water permeability in collecting ducts of kidney, high concentrations= vasoconstictor.
ADH release when
high osmotic pressure, reduced blood volume, and reduced MAP
thromboxane A2
prostaglandin vasoconstrictor, causes platelet aggregation and vasoconstriction
endothelin
ET-1 split from ET-1 by endothelin converting enzyme, long lasting vasoconstrictor
Beta 2 adrenergic receptors
vasodilation when bind E
Bradykinin
A nonapeptide that acts by stimulating nitric oxide and prostacyclin formation by the vascular endothelium.
Involved in inflammation
Destroyed by angiotensin-converting enzyme
serotonin
In platelet granules.
Concentration can increase locally after platelet activation.
Effects complex, depending on dose, experimental conditions, animal species and vascular state.
histamine
Can be a powerful dilator of arterioles, except in the lungs,where it increases PVR
Increases capillary permeability (e.g. to proteins)
Important in inflammation and anaphylactic shock,
where it is released by mast cells.
prostacyclin
produced by the vascular endothelium by prostacyclin synthase used to treat PHT
antagonistic to thromboxane A2
NO
Apart from its action on the vasculature, it also inhibits platelet adhesion, NO is continually produced by nitric oxide synthase in the vascular endothelium,
vascular endothelium source of
prostacyclin (vd), NO (vd) and endothelin (vc)
Parasympathetics
Heart (mainly rate)
Blood vessels: vasodilation in the blush areas and genitals (penile erection is via the intermediary nitric oxide).
sympathetic branch
Controls distribution of cardiac output by vasoconstriction, mainly in the splanchnic and cutaneous circulations.
Regulates mean arterial pressure by acting on the:
a. Heart (cardiac output) (beta 1)
b. Blood vessels (SVR,
capacity) (alpha 1)
c.Volume, via the kidneys
(affects cardiac output)
Angiogenesis
formation of new blood vessels: ischemic tissue, hypoxic wounds, embryogenesis, menstrual cycle.
unregulated angiogenesis
tumor growth, arthritis, diabetic retinopathy, retinopathy of prematurity.
endogenous angiogenesis inhibitors
prevent corneal neovascularization.
angiogenic factors
Synthesis and release of angiogenic factors is driven by low oxygen – high oxygen suppresses them.
MAP regulated by sympathetics (raise MAP)
cardiac output (beta 1), total peripheral resistance (arterioles, alpha 1), capacity (veins and venules alpha 1) and blood volume (renin-angiotensin II-ADH)
baroreceptor reflex (volume depletion)
activator of sympathetic nervous system. critical for
blood pressure homeostasis.Stretch receptors in the carotid sinuses (less importantly the aortic arch) communicate via Hering’s nerve (branch of IX) with neurons in the nucleus tractus solitarius.
NTS is the integrating hub, and modulates the activity of sympathetic and parasympathetic (vagal) neurons in the medulla.
baroreceptor reflex protect against
FALL in MAP, does provide against protection for hypertension
when blood pressure rises….?
impulses from baroreceptor increases in frequency, reducing sympathetic vasoconstriction tone
when blood pressure decreases?
baroreceptor reduce their firing rate , increasing vasomotor tone and causes constriction of veins and arterioles
Shy-Drager
Multiple system atrophy with orthostatic hypotension.A progressive disorder of the CNS and ANS for which there is no cure. Orthostatic hypotension is the first sign of autonomic system failure
orthostatic hypotention patient
supine: 120/74, sitting: 98/54, standing: 84/48
Bainbridge reflex (volume loading)
sometimes called the atrial reflex, is an increase in heart rate and renal vasodilation due to an increase in central venous pressure operating on receptors located on the low pressure side of the circulation.
atrial natriuretic peptide
secretion caused from atrial distension from increased venous pressure. inhibits ADH, renin and aldosterone secretion
renin-aldosteron-angiotensin system
Most important action to control plasma volume. Takes several hours for pathophysiological expression, as might occur in the setting of hemorrhage or MI
Antidiuretic, vasoconstriction
aldosterone
prevents sodium from excretion by promoting sodium reabsorption in distal and collecting tubules of kidneys, causes water retention in response to reduced systemic arterial pressure
