Selective C1 Lesioning Slightly Decreases Angiotensin II Type I Receptor Expression in the Rat Rostral Ventrolateral Medulla (RVLM).

Cardiovascular homeostasis is regulated in large part by the rostral ventrolateral medulla (RVLM) in mammals. Projections from the RVLM to the intermediolateral column of the thoracolumbar spinal cord innervate preganglionic neurons of the sympathetic nervous system causing elevation of blood pressure and heart rate. A large proportion, but not all, of the neurons in the RVLM contain the enzymes necessary for the production of epinephrine and are identified as the C1 cell group.

AT₁ angiotensin II receptor and novel non-AT₁, non-AT₂ angiotensin II/III binding site in brainstem cardiovascular regulatory centers of the spontaneously hypertensive rat.

Spontaneously hypertensive rats (SHR) have an activated brain angiotensin system that contributes to the elevation of blood pressure in this animal model. Physiological and pharmacological studies suggest that hyperactivation of brain AT₁ angiotensin receptors is a major pathophysiological factor. Consistent with these observations, radioligand binding studies indicate widespread up-regulation of brain angiotensin receptors in SHR.

Water deprivation increases angiotensin-converting enzyme but not AT(1) receptor expression in brainstem and paraventricular nucleus of the hypothalamus of the rat.

The rostral ventrolateral medulla (RVLM) is critical to the maintenance of blood pressure. It has been proposed that blood-borne Ang II can influence the RVLM via a neural connection between the circumventricular organs and paraventricular nucleus of the hypothalamus (PVH) and that a component of this pathway is angiotensinergic. A period of water deprivation leads to increased ability of angiotensin type 1 (AT(1)) receptor antagonists to reduce blood pressure when administered into the RVLM and PVH.

Anteroposterior distribution of AT(1) angiotensin receptors in caudal brainstem cardiovascular regulatory centers of the rat.

Angiotensin II acts on Ang II type 1 (AT(1)) receptors in areas of the caudal brainstem involved in cardiovascular regulation. In particular, activation of AT(1) receptors in the rostral ventrolateral medulla (RVLM) has been suggested to contribute to hypertension. However, the characteristics of AT(1) receptors in the RVLM of rat, the species in which the most experimental work has been done, are not well documented.

Angiotensin modulation of rostral ventrolateral medulla (RVLM) in cardiovascular regulation.

The rostral ventrolateral medulla (RVLM) and the presympathetic bulbospinal neurons in this region play a critical role in cardiovascular regulation. However, there is ambiguity regarding the precise anatomical coordinates of the RVLM and much still needs to be learned regarding the regulation and neurochemistry of this region. This brief review discusses some of these issues and focuses on the role of angiotensin-mediated signaling in the RVLM in blood pressure regulation.

Placental insufficiency results in temporal alterations in the renin angiotensin system in male hypertensive growth restricted offspring.

Reduced uterine perfusion initiated in late gestation in the rat results in intrauterine growth restriction (IUGR) and development of hypertension by 4 wk of age. We hypothesize that the renin angiotensin system (RAS), a regulatory system important in the long-term control of blood pressure, may be programmed by placental insufficiency and may contribute to the etiology of IUGR hypertension. We previously reported that RAS blockade abolished hypertension in adult IUGR offspring; however, the mechanisms responsible for the early phase of hypertension are unresolved.

Angiotensin II type 2 receptor gene transfer elicits cardioprotective effects in an angiotensin II infusion rat model of hypertension.

The role of the angiotensin II type 2 receptor (AT2R) in cardiovascular physiology remains elusive. We have developed an in vivo lentiviral vector-mediated gene transfer system to study the physiological functions of the AT2R. Our objectives in this study were to determine whether the AT2R influences cardiac hypertrophy and myocardial and perivascular fibrosis in a nongenetic rat model of hypertension.