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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Renal and femoral venous blood flows are regulated by different mechanisms dependent on alpha-adrenergic receptor subtypes and nitric oxide in anesthetized rats

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Author(s):
Fioretti, Alexandre C. [1] ; Ogihara, Cristiana A. [1] ; Cafarchio, Eduardo M. [1] ; Venancio, Daniel P. [1] ; de Almeida, Roberto Lopes [1] ; Antonio, Bruno B. [1] ; Sato, Monica A. [1]
Total Authors: 7
Affiliation:
[1] ABC, Fac Med, Dept Morphol & Physiol, 2000 Lauro Gomes Ave, BR-09060870 Santo Andre, SP - Brazil
Total Affiliations: 1
Document type: Journal article
Source: VASCULAR PHARMACOLOGY; v. 99, p. 53-64, DEC 2017.
Web of Science Citations: 0
Abstract

Venous and arterial walls are responsive to sympathetic system and circulating substances, nevertheless, very few is known about the venous blood flow regulation simultaneously to arterial vascular beds. In this study, we compared the venous and arterial blood flow regulation in visceral and muscular beds upon injection of different doses of vasoactive drugs which act in arterial vascular beds. Anesthetized adult male Wistar rats underwent to right femoral artery and vein cannulation for hemodynamic recordings and infusion of drugs. Doppler flow probes were placed around the left renal artery and vein, and left femoral artery and vein to evaluate the changes in flood flow. Phenylephrine (PHE) injection (alpha(1)-adrenergic receptor agonist) elicited vasoconstriction in all arteries and veins. Intravenous prazosin (PZS) (1 mg/kg, aradrenergic receptor blocker) caused renal artery vasodilation, but not in the other beds. Vasoconstrictor effect of PHE was abolished by PZS in all vascular beds, except in femoral vein. Phentolamine (PTL) injection (1 mg/kg, alpha(1)/alpha(2)-adrenergic receptor blocker) produced renal artery vasodilation with no change in other beds. After PTL, the vasoconstriction evoked by PHE was abolished in all vascular beds. Sodium Nitroprusside (SNP), a nitric oxide donor, elicited vasodilation in all beds, and after PTL but not post PZS injection, SNP enhanced the vasodilatory effect in femoral vein. Our findings suggest that the vasoconstriction in renal and femoral veins is mediated by different subtypes of a-adrenoceptors. The nitric oxide-dependent vasodilation in femoral vein enhances when a2-adrenoceptors are not under stimulation, but not in the other vascular beds investigated. (AU)