Cultured juxtaglomerular cells cause hypertension by secreting angiotensin.
Cultured JGC contain renin, angiotensin I, angiotensin I-converting enzyme, angiotensin II, and, by implication, the entire RAS. JGC, as transplants, appear to secrete angiotensin II/III directly into the bloodstream to cause hypertension when the renal mass is reduced. There are two main phases of the hypertensive state, an angiotensin-dependent developmental phase and a non-angiotensin-dependent maintenance phase. This model may be useful in attempts to evaluate pro-hypertensive actions of angiotensin other than those due to direct systemic vasoconstriction. Certain of these actions appear to be intrarenal and include the stimulation of sodium reabsorption, a decrease in renopapillary blood flow, the stimulation of prostaglandin synthesis, and a constraint on the antihypertensive function of the RIC.
D000804:Angiotensin II / Q000097:blood / Q000378:metabolism*; D000805:Angiotensin III / Q000097:blood; D000818:Animals; D002216:Captopril / Q000494:pharmacology; D002478:Cells, Cultured; D006973:Hypertension / Q000209:etiology*; D007606:Juxtaglomerular Apparatus / Q000166:cytology / Q000378:metabolism*; D009392:Nephrectomy; D051381:Rats; D012504:Saralasin / Q000494:pharmacology
D000804:Angiotensin II; D000805:Angiotensin III; D002216:Captopril; D012504:Saralasin