Lecture 17: CVS Regulation 1 Flashcards
Local controls of CV regulation
Mechanisms by which organs/tissues alter their own arteriolar resistance, INDEPENDENT of nerves and hormones
Active hyperemia
Refers to an increase in blood flow to a region due to increased metabolic activity; caused by arteriolar dilation
Local chemical changes inducing active hyperemia
Low pO2, high pCO2, high H+, high adenosine (ATP use), high K+ (AP firing), high eicosanoids (p-lipid breakdown); increased bradykinin, increased NO (endothelium)
Bradykinin
Locally generated peptide, potent vasodilator. Kallikrein cleaves circulating kininogen to bradykinin.
Kallikrein
Produced locally with increased metabolic rate, or secreted as prekallikrein by the liver.
Flow autoregulation
Maintenance of constant blood flow despite changes in blood pressure
Mechanisms of flow autoregulation
- Metabolic factors just like with active hyperemia
- Myogenic response
Myogenic response
Mechanism of flow autoregulation. Smooth muscle stretch receptors adjust tone accordingly with changes in vessel stretching to maintain a constant blood flow (less stretch -> less tone/contraction, more stretch -> more tone)
Reactive hyperemia
Phenomenon of profound transient increases in blood flow after restoring completely occluded blood supply. Extreme form of active hyperemia
Extrinsic controls of CV regulation
Aka reflex controls; hormonal + neural innervation
ANS innervation of arterioles
Sympathetic only. NE -> α adrenergic receptors -> vasoconstriction; β in heart.
Innervation always occurs at a basal level/tone which is increased or decreased.
Purpose of intrinsic controls vs extrinsic controls
Intrinsic controls coordinate local needs, while extrinsic reflex controls are concerned with serving the whole body.
ANS non-cholinergic/non-adrenergic innervation of CV
These neurons release other vasodilators e.g. NO, found in places like enteric NS or penis/clitoris (drug targets for viagra/cialis.
Hormonal CVS regulation
Epi -> β2 receptors -> dilation, especially in sk. muscle arterioles
Epi -> α receptors -> vasoconstriction
Angiotensin/vasopressin -> vasoconstriction
ANP -> dilation
Endothelial paracrine secretions
NO, Prostacyclin, Endothelin-1
Endothelial NO secretion
NO is continually secreted at a basal level by endothelial cells and increases rapidly in response to many reflex/local controls
Endothelial prostacyclin secretion
aka prostaglandin I2 (PGI2); low basal level but can increase significantly for vasodilation
Endothelin-1
ET-1 is a vasoconstrictor that is usually paracrine but can also act as a hormone at high enough concentration
Overall CVS regulatory scheme
-Higher centers
-Cardiovascular Control Center (CVCC) in lower pons, medulla)
-Effectors (arterioles, veins, heart)
-Sensors (large arteries, heart)
Myogenic response mechanism
Distention induces opening of Ca++ stretch channels, which induces more Ca++ release from sm. muscle SR -> increase of tone w/ stretch
Important factors for smooth muscle contractility
- Intracellular Ca++ levels (influences MLCK activity)
- K+ conductance
- Direct inhibition of contractile proteins
Cardiovascular Control Center regions
- Nucleus Tractus Solitarius (NTS)
- Vagus nerve cell bodies (X, parasymp.)
- Depressor area (D)
- Pressor area (P)
Depressor and pressor areas of CVCC
Converge on pre-ganglionic sympathetic neurons and influence downstream post-GSN stimulation of effectors via NE. Depressor = inhibitory, pressor = excitatory
CVCC regulation of veins
Veins are the primary capacitance vessels; increase in venous pressure (w/ symp. stim.) increases venous return, helping redistribute blood.
CVCC regulation of the heart
Parasymp. and symp. are in opposition, e.g. vagal ACh lowers HR, symp. stim. increases HR. Both have tone but vagal dominates at rest. Contractility is primarily controlled by sympathetic tone.
