Enhanced Ca2+ response to AVP in preglomerular vessels from rats with genetic hypertension during different hydration states.

Exaggerated arginine vasopressin (AVP)-induced calcium signaling and renal vasoconstriction, characteristic in young spontaneously hypertensive rats (SHR) during euvolemia, are related to greater amounts of V1a receptor mRNA and V1a protein in preglomerular resistance arterioles. The present study determined whether V1a receptor density and calcium signal transduction in the renal vasculature of young SHR is regulated appropriately during physiological changes in hydration state. [3H]AVP ligand binding documented two- to threefold greater density of V1a receptors in euvolemic SHR vs.

Enhanced response to AVP in the interlobular artery from the spontaneously hypertensive rat.

Arginine vasopressin (AVP) induces exaggerated intracellular free calcium (Cai2+) responses in preglomerular smooth muscle cells from young spontaneously hypertensive rats (SHR) due to increased density of the AVP V1a receptor. The intention of the present paper was to examine the relative contribution of afferent arterioles (AA) and interlobular artery (ILA) in AVP- and norepinephrine-induced calcium signaling. The kidneys were perfused with agar solution in vivo, and thin cortical slices were enzyme digested to produce isolated agar-filled vascular fragments.

Age-dependent regulation of vasopressin V1a receptors in preglomerular vessels from the spontaneously hypertensive rat.

Experiments were performed to get insight into the role of AVP receptor V(1a) regulation with age, i.e., during development and maintenance of high blood pressure.