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