Vasopressin and angiotensin II receptors in rat aortic smooth muscle cells in culture

Abstract

Rat aortic smooth muscle cells were isolated and maintained in primary culture. After 2-3 days, cells recovered their contractile phenotype and could be induced to contract in response to vasopressin and angiotensin II. Vasopressin- and angiotensin-specific binding sites were detected on these cells, using tritiated Lys8-vasopressin, Asn1-Val5-angiotensin II, and Sarc1-Ile8-angiotensin II. Vasopressin binding sites had Kd values of 30 and 12 nM for Lys8-and Arg8-vasopressin, respectively, and a maximal binding capacity of 25,000 sites/cell. They displayed several of the expected characteristics of vasopressin receptors involved in the vasopressor response in vivo. A highly significant correlation was found between the relative agonistic or antagonistic vasopressor potencies of a series of vasopressin structural analogues and their relative abilities to inhibit [3H]vasopressin binding to aortic smooth muscle cells. Specific binding sites for Asn1-Val5-angiotensin II and Sarc1-Ile8-angiotensin II had the following characteristics: Kd = 2.3 and 1.3 nM, respectively; maximal capacity: 50,000 sites/cell. Vasopressin and angiotensin did not modify the intracellular cyclic AMP content of aortic smooth muscle cells.

Arginine Vasopressin Enhances Sympathetic Constriction Through the V 1 Vasopressin Receptor in Human Saphenous Vein

“…In contrast, the selective V 1 receptor antagonist d(CH 2 ) 5 Tyr(Me)AVP inhibited the amplifying effects of AVP on electrical field stimulation and norepinephrine-induced contractions in a concentration-dependent manner. In addition, the selective V 1 receptor agonist [Phe, 2 Orn 8 ]-vasotocin induced potentiating effects similar to those observed in the presence of AVP. Therefore, the results exclude a role for V 2 receptors in the potentiating effects of AVP and are consistent with the hypothesis that V 1 receptor stimulation in the absence of direct contraction is followed by enhancement of responses to both endogenous and exogenous norepinephrine.…”

“…First, the selective V 2 receptor agonist desmopressin did not modify responses to electrical field stimulation. On the other hand, the V 2 receptor antagonist [d(CH 2 ) 5 , D-Ile, 2 Ile, 4 Arg 8 ]-vasopressin did not affect the potentiation induced by AVP. In contrast, the selective V 1 receptor antagonist d(CH 2 ) 5 Tyr(Me)AVP inhibited the amplifying effects of AVP on electrical field stimulation and norepinephrine-induced contractions in a concentration-dependent manner.…”

“…To determine whether V 2 receptors are involved in the effects of AVP on field electrical stimulation, frequencyresponse relationships were obtained in the absence and in the presence of the V 2 Blockade of neuronal catecholamines reuptake by cocaine (10 Ϫ6 mol/L) had no effect on the potentiating effects of AVP on electrical field stimulation (Fig 2C). …”

“…[1][2][3] In human vessels, AVP causes powerful V 1 receptor-mediated constriction in isolated mesenteric, 4,5 cerebral, 6,7 and renal 8 arteries. This effect is endothelium independent and due to direct stimulation of receptors located on smooth muscle cells.…”

Similarity of vasopressin receptors in seminal vesicles and renal medulla of pigs

“…Vasopressin receptors have been classified into two different subtypes, the calcium-dependent VI receptors, present in blood vessels (Penit et al, 1983) and liver (Cantau et al, 1980), and the cyclic AMP-dependent V2 receptors, present in the medullary portion of the kidney (Bockaert et al, 1973).…”