Local Control of Blood Flow and Long Term Regulation of Blood Pressure Flashcards
Summary of factors affecting vessel diameter:
How do endothelium-dependent vascular smooth muscle regulation occur?
How is long-term blood pressure regulation maintained?
What are the four major mechanisms of blood flow regulation?
True or False:
Terminal arterioles has the highest relative sensitivity in terms of autoregulatory myogenic & metabolite responsiveness of smooth muscle cells to stimuli.
True
Describe the myogenic reflex response
In the myogenic response, as pressure increases, ht happens to the vascular resistance? What happens to the blood vessel diameter?
How do tissues individually maintain basal myogenic tone & regulate blood flow?
Through local autoregulatory mechanisms
What are some local auto-regulatory mechanisms that cause vasodilation?
What are some local auto-regulatory mechanisms that cause vasoconstriction?
What is hyperemia?
TRANSIENT (temporary) increase in organ blood flow; due to a build up metabolites that induce vasodilation.
Active hyperemia = increase in organ blood flow due to increase in metabolic activity/rate (such as exercise); causes influx in oxygen, which causes vasodilation to a maximum point as shown in the graph.
Reactive hyperemia = increase in organ blood flow due to period of arrested blood flow (like wearing rubberband that cuts of circulation then taking it off.
Release stimulated by hypoxia, shear stress, catecholamines, ADH and Ang II.
Initial stimulation causes transient vasodilation due to initial endothelial ETB activation which triggers nitric oxide (NO) release, and hypotension, followed by prolonged vasoconstriction via ETA binding to & activating the Gq-Ip3-Ca2+ signal cascade pathway (intracellular calcium release causes smooth muscle contraction) & hypertension
Potent coronary vasodilator; Net effect is an increase in HR due to baroreceptor reflex; cAMP is one of my intermediates
What am I?
Adenosine
Produced in the lumen of the blood vessels during inflammation & I bind to my receptor on the surface endothelial cells lining the lumen; activated by Kallikrein; initiates a signal cascade that leads to NO release from endothelial cells, which activates the cGMP signaling cascade in vascular smooth muscle cells, causing vasodilation.
What am I?
Bradykinin
What are the vascular actions of nitric oxide?
Listed below:
NO signals cGMP signaling pathway
List the major vasoconstrictive & vasodilator substances
What is the importance of the Renin-Angiotensin Vasoconstrictor System?
Has a pressure compensating effect that helps the body recover after severe hemorrhage; raises arterial pressure quickly after blood loss
Describe how the Renin-Angiotensin-Aldosterone System (RAAS) works.
- Kidney responds to stimuli:
- increased sympathetic signal
- decreased blood pressure
- decreased sodium delivery to distal tubule (sodium loss/excretion) - Kidney responds by increasing sodium and water reabsorption in collecting ducts &distal tubules, which increases blood volume & cardiac output.
- The kidney will also activate Renin
- Renin leads to the production of Angiotensin 1
- Angiotensin 1 will interact with ACE molecule to synthesize Angiotensin 2.
- Angiotensin 2 will then cause an increase in systemic vascular resistance (vasoconstriction), & an increase in arterial pressure.
What are the sites of modulation/regulation of the Renin-Aldosterone-Angiotensin System?
What receptor does Angiotensin 2 use?
At1 receptor
How does antidiuretic hormone/vasopresin/avp increase arterial pressure?
What are the actions of atrial natriuretic peptide (ANP)?
Reduce blood pressure & blood volume (opposite of angiotensin & ADH & RAAS); promotes vasoconstriction;
Synthesized & stored in the atria of the heart.
BNP is similar but synthesized & stored in the ventricles of the heart & in the brain
Lecture Summary
