Participation of the angiotensinergic and vasopressinergic mechanisms in the maintenance of cardiorespiratory parameters in sodium depleted rats

Fernanda Cardoso; Michele Thaís Fávero; Nathalia Vieira Veríssimo; Miguel Furtado Menezes; José Vanderlei Menani; Patricia Maria de Paula

doi:10.1016/j.heliyon.2022.e12221

Participation of the angiotensinergic and vasopressinergic mechanisms in the maintenance of cardiorespiratory parameters in sodium depleted rats

Heliyon. 2022 Dec 13;8(12):e12221. doi: 10.1016/j.heliyon.2022.e12221. eCollection 2022 Dec.

Authors

Fernanda Cardoso¹, Michele Thaís Fávero¹, Nathalia Vieira Veríssimo¹, Miguel Furtado Menezes¹, José Vanderlei Menani¹, Patricia Maria de Paula¹

Affiliation

¹ Department of Physiology and Pathology, School of Dentistry, São Paulo State University - UNESP, 14801-903 Araraquara, SP, Brazil.

Abstract

Changes in blood volume can be caused by different conditions, such as vomiting, diarrhea, alteration of sodium intake, trauma, or the use of diuretics, which can lead to severe health deterioration. Understanding the mechanisms involved in the maintenance of physiological parameters and the hydroelectrolytic balance of the human body during hypovolemia, can help with preventing and handling these high-risk situations. Hence, this study investigated cardiorespiratory [mean arterial pressure (MAP), heart rate (HR), pulmonary ventilation (VE)] and blood parameters, of sodium depleted rats with furosemide and the roles of the central and peripheral renin-angiotensin and the peripheral vasopressinergic systems in controlling blood pressure in these animals. Different groups under the same conditions received subcutaneous (s.c.) injections of furosemide (diuretic/saliuretic) or vehicle, intracerebroventricular (i.c.v.) or intravenous (i.v.) injections of losartan [angiotensin II (ANG II) AT1 receptor antagonist] or saline, and i.v. injections of Manning compound (AVPX, vasopressin V1 receptor antagonist). Sodium depletion increased the VE (708 ± 71, vs. normovolemic: 478 ± 40 mL/min/kg body wt) and did not modify baseline mean arterial pressure (104 ± 4, vs. normovolemic: 105 ± 4 mmHg) and heart rate (334 ± 20, vs. normovolemic: 379 ± 13 bpm). The i.v. losartan (10 mg/kg of body wt) treatment significantly reduced MAP in all groups and elevated HR, with a greater impact in sodium depleted rats before repletion. On the other hand, the i.c.v. losartan (3.3 μg/kg of body wt) and i.v. AVPX (10 μg/kg of body wt) treatments did not alter the MAP and HR in control, sodium depleted, and sodium repleted rats. These results indicate that sodium depletion affects cardiorespiratory control increasing baseline ventilation and peripheral angiotensinergic mechanisms are relevant for maintaining cardiovascular parameters in sodium depleted rats. Besides, this study suggests vasopressin V1 receptors do not participate in the maintenance of MAP and HR in sodium depleted animals with furosemide.

Keywords: Angiotensin II; Central and peripheral cardiovascular regulation; Furosemide; Sodium depletion; Vasopressin; Ventilation.