Key result
Acute injection of Ang 1-7 into the PVN increased blood pressure by about 15 mmHg and heart rate by about 14 beats/min, effects that were attenuated or reversed by specific receptor antagonists.
Why the study?
The mechanisms and receptors contributing to the pressor and tachycardic effects of acute central administration of Ang 1-7 are not fully understood.
The central pressor and tachycardic effects of Ang 1-7 in the PVN are mediated by glutamate, vasopressin, GABA A, and thromboxane receptors, as well as oxidative stress.
Central Ang 1-7 pressor effects in rodents remain mechanistically unclear; leaves open human receptor targets and relevance.
Although angiotensin 1-7 (Ang 1–7) and its role as a part of the “protective” axis of the renin-angiotensin system are well described in the literature, the mechanisms of its angiotensin II-like pressor and tachycardic effects following its acute central administration are not fully understood. It was the aim of the present study to examine which receptors contribute to the aforementioned cardiovascular effects. Ang 1–7 and antagonists for glutamate, GABA, vasopressin, thromboxane A 2 (TP), α 1 -adrenergic, and P2X purinoceptors or modulators of oxidative stress were injected into the paraventricular nucleus of the hypothalamus (PVN) of urethane-anesthetized male Wistar rats. Acute injection of Ang 1–7 into the PVN increased blood pressure (BP) by about 15 mmHg and heart rate (HR) by about 14 beats/min. After preinjection with bicuculline (GABA A receptor antagonist), CNQX + D-AP5 (AMPA/kainate and NMDA receptor antagonists) and SQ29548 (TP receptor antagonist) the BP and HR reactions to Ang 1–7 were attenuated or abolished. The vasopressin V 1A and V 1B receptor antagonists conivaptan and nelivaptan, and the NADPH oxidase inhibitor apocynin even reversed the pressor and tachycardic effects of Ang 1–7. Antagonists of P2X (PPADS) and α 1 -adrenergic receptors (prazosin), the free radical scavenger tempol and the superoxide dismutase inhibitor DETC did not modify the cardiovascular effects of Ang 1–7. The (Mas receptor-related) rise in BP and HR evoked by Ang 1-7 administered to the rat PVN is linked to glutamate, vasopressin, GABA A and thromboxane receptors, and to oxidative stress, but does not seem to involve α 1 -adrenergic or P2X receptors. • Ang 1–7 injected into the PVN increases blood pressure via various receptors. • Pressor effect of Ang 1–7 involves glutamatergic and vasopressinergic pathways. • GABA A , glutamate, vasopressin and TP receptors mediate in pressor effect of Ang 1-7. • Pressor effect of Ang 1–7 does not involve α 1 -adrenergic and P2X receptors. • The protective action of Ang 1–7 is weakened by its central pressor effect.
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Mińczuk et al. (2024) studied this question. Angiotensin 1-7 injection into the paraventricular nucleus of the hypothalamus vs. Various receptor antagonists and modulators was evaluated on Blood pressure and heart rate. Acute injection of Ang 1-7 into the PVN increased blood pressure by about 15 mmHg and heart rate by about 14 beats/min, effects that were attenuated or reversed by specific receptor antagonists.
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