Cardiovascular effects of ventrolateral periaqueductal gray (vlPAG) AT1 receptors in normotensive and hemorrhagic rats.

OBJECTIVES

The ventrolateral periaqueductal gray (vlPAG) regulates cardiovascular function. Given the presence of Angiotensin II (AngII) and its AT1 receptors (AT1R) in the vlPAG, this study investigated their central and peripheral roles in cardiovascular control during normotensive and hemorrhage (Hem) conditions.

MATERIALS AND

METHODS

Saline, three doses of AngII (0.1, 0.2, and 0.3 nmol) were microinjected into the vlPAG. The AT1R blocker Losartan (Losa) was microinjected alone and before AngII in normotensive and Hem conditions. The peripheral mechanisms of AngII were examined by intravenous injection of hexamethonium (Hexa, a ganglion blocker) and atropine (Atro, a muscarinic receptor blocker), alone and before AngII (0.3 nmol), in both normotensive and Hem conditions. Time course and maximal changes (Δ) of mean arterial pressure (MAP), systolic blood pressure (SBP), and heart rate (HR) were recorded by the PowerLab apparatus and analyzed.

RESULTS

Higher doses of AngII significantly increased HR, SBP, and MAP (P<0.05-P<0.001) than saline. Losa attenuated these effects. Hexa significantly attenuated the pressor effect of AngII (P<0.001), while Atro increased HR (P<0.001). Hem decreased SBP/MAP and increased HR (P<0.01); these responses were augmented by AngII, and Losa blocked this AngII effect. Hexa reduced the cardiovascular improvement induced by AngII during Hem, and Atro enhanced the AngII-induced tachycardia.

CONCLUSION

AngII in the vlPAG stimulates cardiovascular activity via AT1R in both normotensive and Hem conditions. Furthermore, these peripheral effects of AngII are primarily mediated through sympathetic nervous system activation.