Mechanisms involved in the cardiovascular effects caused by acute osmotic stimulation in conscious rats

Abstract

Both the autonomic nervous system and the neuroendocrine system are activated by osmotic stimulation (OS) evoking cardiovascular effects. The current study investigated the mechanisms involved in the cardiovascular responses evoked by an acute osmotic stimulus with intraperitoneal (i.p.) injection of either isotonic (0.15 M NaCl) or hypertonic saline (0.6 M NaCl) in conscious rats. Hypertonic saline increased mean arterial pressure (MAP) and heart rate (HR) for 30 min, as well as plasma osmolality and sodium content. Urinary sodium and urinary volume were also increased. Pretreatment with the ganglion blocker pentolinium (i.v.) did not affect the pressor response, but significantly decreased the tachycardic response caused by OS. Pretreatment with the V₁-vasopressin receptor antagonist dTyr(CH₂)₅(Me)AVP (i.v.) reduced the pressor response, without affecting the tachycardic response evoked by the hypertonic OS. Neither the pressor nor the tachycardic response to OS was affected by pretreatment with either the oxytocin receptor antagonist atosiban or the α1-antagonist prazosin. Pretreatment with the β1-antagonist atenolol had no effect on the pressor response, but markedly decreased the tachycardic response evoked by OS. Results indicate that i.p. hypertonic OS-evoked pressor response is mediated by the release of vasopressin, with a minor influence of the vascular sympathetic input.

LAY SUMMARY

• Increased plasma osmolality, such as that observed during dehydration or salt intake, is a potent stimulus yielding to marked cardiovascular and neuroendocrine responses. The intraperitoneal (i.p.) injection of hypertonic saline solution is a commonly used animal model to cause a sustained increase in plasma osmolality, leading to a cardiovascular response characterized by sustained blood pressure and heart increases, whose systemic mechanisms were presently studied. Our findings indicate that the pressor response to the i.p. osmotic stimulus (OS) is mediated mainly by the release of vasopressin into the blood circulation with a minor or even the noninvolvement of the vascular sympathetic nervous system, whereas activation of the sympathetic-cardiac system mediates the tachycardic response to OS.

Keywords:

• Osmotic stimulation
• vasopressin
• autonomic nervous system
• neuroendocrine
• mean arterial pressure
• heart rate

Acknowledgements

The authors wish to thank Ivanilda A. C. Fortunato for technical help. E. A. T. Fortaleza is a post-doctoral fellow in the Department of Pharmacology of the School of Medicine of Ribeirão Preto-USP [São Paulo Research Foundation (FAPESP) 2012/18556-2]; [National Council for Scientific and Technological Development (CNPq) 167443/2017-8; PDJ 405584/2017-2]. Ivaldo Jesus Almeida Belém-Filho is a PhD student [FAPESP 2016/25502-7]. Cristiane Busnardo is a post-doctoral fellow in the Department of Pharmacology of the School of Medicine of Ribeirão Preto-USP [Postdoctoral National Program (PNPD) of Coordination for the Improvement of Higher Education Personnel (CAPES); Gislaine Almeida-Pereira is a post-doctoral fellow in the Department of Physiology of the School of Medicine of Ribeirão Preto-USP [FAPESP 2014/25005-8].

Disclosure statement

The authors report no conflicts of interest.

Additional information

Funding

Conselho Nacional de Desenvolvimento Científico e Tecnológico. (CNPq); Fundação de Amparo à Pesquisa do Estado de São Paulo. (FAPESP); Coordenação de Aperfeiçoamento de Pessoal de Nível Superior. (CAPES).