. Ans. d. VasodilationAngiotensin II causes vasoconstriction (most potent or - 4-S times more than noradrenaline on weight basis)."Cotonic motility is minimal in fasting period. Eating stimulates colonic contractions. Fat component of meal is major stimulus to colonic contractions. Protein ingestion inhibits colonic contraction. Maximum postprandial increase in motility is seen in sigmoid colon > descending colon > transverse colon"Actions of Angiotensin IIBlood Vessels(AT1A receptors)Brain(AT1a receptors)Adrenal Cortex(AT1B receptors)Others* Potent arteriolar (Vaso) constrictor causing:-Rise in systolic and diastolic BP-Rise in total peripheral resistance* Its pressor activity is decreased in cirrhosis and in Na* depleted individuals. Because circulating angiotensin II is increased in those conditions, which down regulates angiotensin receptors in vascular smooth muscle* It does not penetrate blood brain barrier, but triggers responses by acting on circum ventricular organs (out side BBB)* Area postrema is primarily responsible for pressure potentiation. Angiotensin II acts here to decrease the sensitivity of baroreflex* Dipsogenic effect (i.e. Increase thirst or water intake) is due to action of subfornical organ and organum vasculosum of lamina terminalis.* | Antidiuretic hormone(ADH) or vasopressin) from posterior pituitary* | ACTH* Increase secretion of aldosterone which:- Promotes Na and water reabsorption0- Expands ECF (leading to CO)- Facilitates K+ excretion* Direct effect on PCT to increase Na+ reabsorption by increasing Na+ - H+ exchange* Contraction of mesangial cells with resultant decrease in GFR* Direct action on post ganglionic sympathetic neurons facilitates release of norepinephrine