Involvement of the AT1 receptor in the venoconstriction induced by angiotensin II in both the inferior vena cava and femoral vein

Abstract

Although angiotensin II-induced venoconstriction has been demonstrated in the rat vena cava and femoral vein, the angiotensin II receptor subtypes (AT(1) or AT(2)) that mediate this phenomenon have not been precisely characterized. Therefore, the present study aimed to characterize the pharmacological receptors involved in the angiotensin II-induced constriction of rat venae cavae and femoral veins, as well as the opposing effects exerted by locally produced prostanoids and NO upon induction of these vasomotor responses. The obtained results suggest that both AT(1) and AT(2) angiotensin II receptors are expressed in both veins. Angiotensin II concentration-response curves were shifted toward the right by losartan but not by PD 123319 in both the vena cava and femoral vein. Moreover, it was observed that both 10(-5)M indomethacin and 10(-4)M L-NAME improve the angiotensin II responses in the vena cava and femoral vein. In conclusion, in the rat vena cava and femoral vein, angiotensin II stimulates AT(1) but not AT(2) to induce venoconstriction, which is blunted by vasodilator prostanoids and NO.

Venous endothelial function in cardiovascular disease

“…It is well known that contractile agonists also stimulate the release of EDRFs to counteract their vasoconstrictor effect. Increasing concentrations of Ang II induce contraction in isolated inferior vena cava, femoral, superior mesenteric, and portal veins of healthy rats, which is partially counterbalanced by NO since NO synthase inhibition enhances vasoconstriction induced by this peptide [ 44 , 45 ]. Intriguingly, in the primary culture of rat vena cava and portal vein endothelial cells, Ang II increased NO production in the vena cava, but not in the portal vein cells [ 41 ].…”

“…However, the influence of COX-derived metabolites on Ang II-induced contraction is still not a consensus. In isolated vena cava and femoral vein, Ang II-induced venoconstriction was potentiated in the presence of a non-selective COX inhibitor [ 44 ], whereas COX metabolites did not affect the Ang II response in isolated superior mesenteric and portal veins [ 45 ]. Intriguingly, Ang II increased the production of both PGI 2 and PGF 2α in the primary culture of vena cava endothelial cells, and only enhanced the PGF 2α production in the portal vein [ 41 ].…”

Exercise training attenuates angiotensin II‐induced vasoconstriction in the aorta of normotensive but not hypertensive rats

“…On the other hand, Ang II‐induced vasoconstriction is strictly modulated by endothelium‐derived mediators. Nitric oxide (NO), prostanoids and hyperpolarizing substances produced by the endothelium may act in isolation or in combination to modulate the vascular responses to Ang II (Chies et al., 2017; Chies, Rossignoli, Baptista, de Lábio, & Payão, 2013; da Silva, de Souza Rossignoli, Carrillo‐Sepúlveda, Barreto‐Chaves, & Chies, 2011; Tirapelli et al., 2005). Thus, modifications in the endothelial functioning, accompanied or not by changes in the smooth muscle cells or the extracellular matrix, may lead to hypertension and/or contribute to its maintenance.…”