Neurohumoral Mechanisms Involved in the Hypertensive Response Elicited by Bilateral Carotid Occlusion in Conscious Intact or Chronically Sympathectomized Rats

Abstract

Bilateral carotid occlusion (BCO) increases the sympathetic drive to the circulatory system in conscious intact rats, producing a hypertensive response characterized by two components, i.e., an initial peak followed by a sustained response of lower intensity. The neurohumoral mechanisms involved in the hypertensive response to BCO were evaluated in conscious intact (INTACT) or chronic guanethidine sympathectomized (SYMPX) rats. To accomplish this, the receptor antagonists, prazosin for α₁‐adrenergic receptor, losartan for AT₁ angiotensin II receptor and [d(CH₂)5Tyr(Me)AVP] for vascular V₁ vasopressin receptor were used. A saline control group was studied as well. Conscious rats were equipped with cuffs around the common carotid arteries plus arterial and venous catheters. The results indicate that the sympathetic nervous system is the main mechanism controlling the basal arterial pressure in conscious INTACT rats, whereas in chronically SYMPX rats the renin–angiotensin system plays this role. In INTACT rats prazosin abolished the initial peak and blunted the sustained hypertensive response due to BCO, while the other antagonists exhibited no effect. SYMPX rats did not present the initial peak but displayed an enhanced sustained response, which was blunted by prazosin or the vasopressin antagonist. In conclusion, activation of the sympathetic drive is responsible for both the initial peak and the sustained hypertensive response due to BCO in conscious INTACT rats. On the other hand, vasopressin acting in concert with the sympathetic nervous system, plays a key role in the potentiation of the sustained hypertensive response due to BCO in conscious chronically SYMPX rats.

• Carotid occlusion
• Sympathetic nervous system
• Renin–angiotensin system
• Vasopressin
• Chemical sympathectomy