L16 - The Cardiac Conduction system Flashcards
Summarise the metabolic control concept
- Increase in metabolic activity leads to…
- Increased release of metabolic byproducts…
- Causes increased resistance vessel dilation
- Permitting increased BF
- Resulting in increased Oxygen and nutrient supply
Resistance vessels are sensitive to metabolites found where?
Extracellular fluid and oxygen.
Vascular smooth muscle cells dilate, increasing blood flow
Myogenic control concept
IF
- intraluminal pressures rise
- then resistance vessels may constrict
- contraction mediated by stretch activated Ca2+ channels in VSMC membranes
IF arterial pressure were to rise suddenly…
Flow will increase
- metabolites washed away faster than produced
- resistance vessels constrict reflexively
Sudden drop in arterial pressure may lead to…
Reflex vasodilation
Reactive hyperaemia
Period of increased BF that follows transient ischaemia, caused by arterial occlusion.
What hormones help control blood flow? (4)
- Epinephrine
- atrial natriuetic peptide
- angiotensin II
- ADH
Briefly, what modulated release of ADH?
- released from posterior pituitary
- when tissue osmolarity rises or blood volume falls.
Where does ADH bind?
Binds to vasopressin V1a receptors n VSMC
V1a receptor couple to IP3 pathway
Angiotensin II
Potent vasoconstrictor.
Appears in blood stream when renal artery pressure falls.
Binds to angiotensin AT1 receptor on VSMC, which couple to the IP3 signaling pathway
Epinephrine
Adrenal medulla, SNS response.
Increase myocardial contractility and HR.
Binds:
- A1 adrenergic receptor VSMC –> V. CCONSTRICTION
- B2 adrenergic receptor –> V.DILATION
What is released by atrial myocytes if they are stretched by high blood volume?
Atrial myocytes will release ANP.
Role of ANP
- vasodilation
- binds to natriuretic peptide receptors, NPR1 on VSMCs
- NPR1 is a guanyl cyclase that relaxes VSMCs by activating protein kinase G.
Summarise what chemicals contribute to endothelial control? (4)
- nitric oxide
- prostaglandins
- endothelins
- endothelium derived hyperpolarising factor
Vasodilators produced by the endothelium
- NO
- Prostacyclin
- Endothelium-derived hyperpolarizing factors
Vasoconstrictors produced in the endothelium
- endothelin
- thromboxane A2
- superoxide
Describe how NO is produced and its action?
- eNOS (constitutive endothelial NO synthase) produces NO.
- diffuses into VSMC
- activated guanylyl cyclase
- causes release of cGMP
- causes protein kinase G activation
- PKG phosphorylated thereby inhibiting myosin light chain kinase
- phosphorylates and increases activity of sarcoendoplasmic retriculum ATPase
- VASODILATION and increased BF
Angina
Caused by inadequate myocardial oxygen supply.
What could be used as treatment for angina and why?
- nitroglycerin (nitrate)
- nitrates break down to release NO in vivo
- causing arerial and venous vasodilation to lower ventricular afterload and preload
Describe action of prostaglandins on vasculature
- many PGE relax VSMC in vascular beds
- PGF and thromboxane A are vasoconstrictors
Describe role of endothelium derived hyper polarising factor
- EDHF opens K+ channels in the plasma membrane of VSMCs
- ensuing membrane hyperpolarisation reducing calcium permeability
- causing intracellular calcium levels to fall
- vasodilation
Action of endothelin
- ET-1 = potent vasoconstrictor binds to ETa receptor on VSMC membrane
- triggers intracellular Ca2+ release via IP3 pathway.
Action of oestrogen on NO?
Oestrogen stimulates NO release from endothelium.
How is Mean arterial pressure mediated?
- changes in circulating BV by modifying renal function.