Role of the organum vasculosum of the lamina terminalis for the chronic cardiovascular effects produced by endogenous and exogenous ANG II in conscious rats

Vieira AA, Nahey DB, Collister JP. Role of the organum vasculosum of the lamina terminalis for the chronic cardiovascular effects produced by endogenous and exogenous ANG II in conscious rats. Am J Physiol Regul Integr Comp Physiol 299: R1564-R1571, 2010. First published September 22, 2010; doi:10.1152/ajpregu.00034.2010.-Endogenous and exogenous circulating ANG II acts at one of the central circumventricular organs (CVOs), the subfornical organ (SFO), to modulate chronic blood pressure regulation. However, at the forebrain, another important CVO is the organum vasculosum of the lamina terminalis (OVLT). In the present study, we tested the hypothesis that the OVLT mediates the hypertension or the hypotension produced by chronic infusion of ANG II or losartan (AT1 antagonist), respectively. Six days after sham or OVLT electrolytic lesion, male Sprague-Dawley rats (280-320 g, n = 6 per group) were instrumented with intravenous catheters and radiotelemetric blood pressure transducers. Following another week of recovery, rats were given 3 days of saline control infusion (7 ml/day) and were then infused with ANG II (10 ng.kg(-1).min(-1)) or losartan (10 mg.kg(-1).day(-1)) for 10 days, followed by 3 recovery days. Twenty-four hour average measurements of mean arterial pressure (MAP) and heart rate (HR) were made during this protocol. Hydromineral balance (HB) responses were measured during the experimental protocol. By day 9 of ANG II treatment, MAP had increased 16 +/- 4 mmHg in sham rats but only 4 +/- 1 mmHg in OVLT lesioned rats without changes in HR or HB. However, the hypotension produced by 10 days of losartan infusion was not modified in OVLT lesioned rats. These results suggest that the OVLT might play an important role during elevation of plasma ANG II, facilitating increases of blood pressure but is not involved with baseline effects of endogenous ANG II.