The pressor effect of angiotensin-(1-7) in the rat rostral ventrolateral medulla involves multiple peripheral mechanisms

OBJECTIVE: In the present study, the peripheral mechanism that mediates the pressor effect of angiotensin-(1-7) in the rostral ventrolateral medulla was investigated. METHOD: Angiotensin-(1-7) (25 pmol) was bilaterally microinjected in the rostral ventrolateral medulla near the ventral surface in urethane-anesthetized male Wistar rats that were untreated or treated (intravenously) with effective doses of selective autonomic receptor antagonists (atenolol, prazosin, methyl-atropine, and hexamethonium) or a vasopressin V1 receptor antagonist [d(CH2)5 -Tyr(Me)-AVP] given alone or in combination. RESULTS: Unexpectedly, the pressor response produced by angiotensin-(1-7) (16 ± 2 mmHg, n = 12), which was not associated with significant changes in heart rate, was not significantly altered by peripheral treatment with prazosin, the vasopressin V1 receptor antagonist, hexamethonium or methyl-atropine. Similar results were obtained in experiments that tested the association of prazosin and atenolol; methyl-atropine and the vasopressin V1 antagonist or methyl-atropine and prazosin. Peripheral treatment with the combination of prazosin, atenolol and the vasopressin V1 antagonist abolished the pressor effect of glutamate; however, this treatment produced only a small decrease in the pressor effect of angiotensin-(1-7) at the rostral ventrolateral medulla. The combination of hexamethonium with the vasopressin V1 receptor antagonist or the combination of prazosin, atenolol, the vasopressin V1 receptor antagonist and methyl-atropine was effective in blocking the effect of angiotensin-(1-7) at the rostral ventrolateral medulla. CONCLUSION: These results indicate that angiotensin-(1-7) triggers a complex pressor response at the rostral ventrolateral medulla that involves an increase in sympathetic tonus, release of vasopressin and possibly the inhibition of a vasodilatory mechanism.

Effect of adrenergic stimulation of the amygdalois complex on water intake

O efeito da noradrenalina, isoproterenol, fentolamina e propanolol, injetados no núcleo basolateral da amigdala, sobre a ingestäo de água, foi investigado em ratos Holtzman. A injeçäo de noradrenalina (40nmol) no complexo amigdalóide (CA) de ratos saciados näo produziu nenhuma mudança na ingestäo de água em ratos saciados (1,93 ñ 0,23 ml/lh). A noradrenalina injetada no CA produziu uma diminuiçäo na ingestäo de água de ratos privados (0,40 ñ 0,19 ml/lh). A injeçäo de isoproterenol no CA de ratos privados näo produziu nenhuma mudança na ingestäo de água em comparaçäo aos controles (11,65 ñ 1,02 e 10,92 ñ 0,88 ml/lh, respectivamente). Quando comparado com valores controles, a fentolamina injetada prévia à noradrenalina bloqueou o efeito inibitório da noradrenalina sobre a ingestäo de água em ratos privados 10,40 ñ 1,31 ml/lh). O propanolol bloqueou o efeito do isorpoterenol em ratos saciados (0,85 ñ 0,49 ml/lh) e também bloqueou a ingestäo água induzida por privaçäo (0,53 ñ 0,38 ml/lh). Tanto em animais saciados quanto em privados, a injeçäo de fentolamina, antes da administraçäo de hexametônio, bloqueou o efeito inibitório do hexametônio na ingestäo de água. Em animais saciados, quando o hexametônio foi injetado sozinho, a ingestäo de água foi de 0,39 ñ 0,25 ml/lh; quando acompanhado de fentolamina, a ingestäo de água foi de 1,04 ñ 0,3 ml/lh. Em ratos privados, o hexametônio sozinho bloqueou a ingestäo de água (0,40 ñ 0,17 ml/lh) e quando injetado com fentolamina produziu uma ingestäo de 9,7 ñ 1,8 ml/lh. Este resultados demonstram claramente a participaçäo de receptores catecolaminérgicos do CA na regulaçäo da ingestäo de água.

Electrical and chemical stimulation of the same hypothalamic loci in relation to agressive behaviour in cats: a comparison study.

Chemitrodes which permit electrical and chemical stimulation of the same hypothalamic loci were implanted in anterior hypothalamic and preoptic regions. These sites were stimulated electrically using biphasic square wave pulse (1 ms, 60 Hz) at a current strength ranging from 150-800 microA to evoke an aggressive response. At lower current strength of 150-200 micro A, defence response, a sort of non-specific response can be elicited from these regions. Increasing the current strength to 400 microA led to the recruitment of affective and somatic components and changed the response pattern either to affective attack or flight. The loci producing affective attack response were localized more laterally and ventrally while the loci producing flight response were located in the dorsomedial regions of the hypothalamus. In this response the animal made a goal-directed attempt to escape through an escape route. Increasing the current strength to 500 microA in the dorsomedial regions changed the flight response to violent flight, which involved vigorous running with unsheathed claws and attacking objects if obstructed. Similar increase in current strength at loci producing affective attack only led to a decrease in the latency of response and made the attack more vigorous. Microinfusion of carbachol in graded doses of 2-15 microgram at all these loci produced a profound affective display. At lower doses of 2 and 5 microgram, only some components of affective display like alertness, pupillary dilation and ear flatness were exhibited. Increasing the dose to 10 micrograms and 15 micrograms led to the recruitment of other affective components like piloerection, salivation, hissing and baring of teeth. Microinfusion of carbachol at all loci producing affective attack on electrical stimulation produced a prononced affective display while microinfusion of carbachol at loci producing flight response led to the development of defence posture. At six loci a typical flight response was obtained while violent flight was never exhibited at any of these sites. Microinfusion of atropine (10 microgram in 1.0 microliter saline) at these loci completely blocked the carbachol induced response. Both somatomotor and affective components were completely inhibited. However, the responses obtained on electrical stimulation were not totally blocked following atropine infusion and some of the somatomotor and affective components could be elicited with higher current strength. These studies indicate the involvement of cholinoceptive mechanisms in the elicitation of hypothalamically induced aggresive behaviour. Microinfustion of hexamethonium bromide, a nicotinic blocker in 50 micrograms doses did not affect the aggressive response.