Key result
In kidneys from genetically hypertensive but not normotensive rats, Y1-receptor activation markedly enhances angiotensin II-mediated renal vasoconstriction by a mechanism involving Gi.
Y1-receptor activation via a Gi-dependent mechanism markedly enhances angiotensin II-mediated renal vasoconstriction in genetically hypertensive rats, suggesting a potential mechanism in the etiology of genetic hypertension.
No takes yet. Share an insight, caveat, or question.
Hypothesis-generating in hypertensive rat models; leaves open human translation or therapeutic targeting.
Dubinion et al. (2005) studied Hypertension. Y1-receptor and Y2-receptor agonists vs. Normotensive rats / basal perfusion pressure was evaluated on Angiotensin II-induced changes in perfusion pressure in isolated, perfused kidneys. In kidneys from genetically hypertensive but not normotensive rats, Y1-receptor activation markedly enhances angiotensin II-mediated renal vasoconstriction by a mechanism involving Gi.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: