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Lecture 37

Cardiovascular Regulation-Hypertension

Local Control non neural factors. dec P leads to dec flow leads to homeostatic tissue response leads to inc flow autoregulation-each organ controls local blood flow
Metabolic Vasodilators active tissues produce vasodilators. ATP use leads to inc adenosine production. adenosine is a strong vasodilator-active hyperemia.
Endothelial Factors paracrines.released from endothelium,affect VSM
Nitric Oxide hormonal/neural activation. inc NO leads to relaxed VSM leads to inc blood flow
Endothelium peptide-constricts VSM. dec flow leads to inc BP. stimulates of E inc gene activity that makes E
Baroreceptors stretch receptors in carotid sinus and aortic arch.changes in BP after baroreceptor activity.
Input to Medulla baroceptors send neurons to medulla in the brain stem
Control of Vasoconstriction/Dilation cardiovascular control center CCC.is in medulla. ccc controls symp and parasymp output.homeostatic short term control of BP. sym: dec BP causes inc baroceptor input causes inc parasymp output causes dec BP (lower HR)
Resetting body adjusts to own "normal" BP. adaptation to prolonged BP change occurs over days
Hypertension chronic elevated BP. mult causes-several small changes cause large inc in BP.
Cardiac Effects hypertrophy against inc load (diastolic pressure) inc oxy use-heart attack when coronaries w/ age inc in systolic pressure inc stroke risk
Essential Hypertension cause unknown,treat symptoms. effective-reduces pathology
Renal Hypertension also called secondary hypertension. dec blood flow to kidneys cause inc kidney renin release. renin converts anglotensinogen to anglotensin 1 (A1). anglotensin converting enzyme ACE in lung capillaries converts A1 to anglotensin 2. and 2 inc blood pressur
Renal Hypertension cont ang 2 is a strong vasoconstrictor and causes aldosteron release from adrenal cortex aldosteron inc na+ reab and h2o reab by kidneys,more volume
In Pregnancy placental factor causes vasoconstriction pre-eclampsia is hypertension during pregnancy. magnesium sulfate treatment lowers BP
Drug Treatments often used in combo. varying side aeffects
Diuretics inc na+ secretion,lowers blood vol/dec BP
ACE Inhibitors block conversion of anglotensin 1 to ang 2
a-Adrenergic Receptor Blockers stops symp constriction of VSM,blocks NE effects.fewer ca2+ channels open,less force
b-Adrenergic Receptor Blocks blocks NE/Epl effects on heart-less ca2+ entry.dec force of cardiac contractions
Calcium Channel Blockers dec VSM contraction,blocks tone
Shock very low BP. loss of blood,toxic vasodilation.reversible shock-can recover from. epinepherine inc BP-side effects sig. irreversible shock-mult organ failure due to low BP. death results.
Created by: danamarie9323