Increased expression of glomerular AT1 receptors in rats with myocardial infarction.

Rats with congestive heart failure demonstrate striking intrarenal vasoconstriction that contributes to reduced renal excretory function. We previously demonstrated that inhibition of angiotensin action reverses intrarenal vasoconstriction in rats 4-6 wk after coronary artery ligation. In the present study we tested the hypothesis that abnormalities in the expression and regulation of glomerular angiotensin receptors contribute to the intrarenal vasoconstriction.

Renal hemodynamics in rats with myocardial infarction: selective antagonism of angiotensin receptor subtypes.

Rats with congestive heart failure demonstrate striking intrarenal vasoconstriction that contributes to reduced renal excretory function. The importance of specific angiotensin II receptor subtypes (AT1, AT2) for mediating changes in renal hemodynamics was studied in anesthetized rats 1 mo after myocardial infarction (MI) created by coronary artery ligation. AT1 antagonism with losartan alone decreased mean arterial pressure (MAP), total peripheral resistance (TPR), and renal resistance (RR) in control and MI rats to a similar extent without affecting renal blood flow (RBF) or RBF as a percentage of cardiac output (%RBF/CO).

Osmolar regulation of endothelin signaling in rat renal medullary interstitial cells.

We tested the hypothesis that endothelin (ET) responsiveness in the renal medulla is modulated by ambient osmolarity. Cultured renal medullary interstitial cells (RMICs) were incubated from 3 to 24 h in isosmolar culture medium (300 mOsm/kg H2O) or media rendered hyperosmolar (600 mOsm/kg H2O) by the addition of urea. Under hyperosmolar conditions, the peak of ET-evoked Ca2+ transient was blunted by 45-58% (P < 0.

Reduced thromboxane receptor affinity and vasoconstrictor responses in placentae from diabetic pregnancies.

Thromboxane has been implicated in the pathogenesis of maternal hypertension in high-risk pregnancies, but potential abnormalities in thromboxane-mediated constriction of fetoplacental vessels has not been examined. Using the isolated perfused fetoplacental cotyledon, we compared the vasoconstrictor responses to a thromboxane mimetic, U46619, in placentae from normal women and women with diabetes mellitus (classes C, D and R). Increases in perfusion pressure in response to bolus injections of U46619 were used to construct dose-response curves.

Endothelin-1 conversion and receptor characterization in human placental arteries.

Endothelin-1-(1-21), a potent pressor peptide, is transcribed as big endothelin-(1-38) and converted to active peptide by endothelin-converting enzyme. The current investigation tested the hypothesis that human fetoplacental blood vessels convert big endothelin-1 to active peptide and that fetoplacental blood vessels respond to endothelin-1 by binding of the peptide to specific receptor sites. In the isolated perfused placental cotyledon the addition of big endothelin-1 to the perfusate caused a time-dependent increase in perfusion pressure that corresponded to the appearance of endothelin-1 in the perfusate.