Interaction of Opioids and Vasopressin in Central Action of Angiotensin II in Consciour Rabbits.

Abstract

It has been demonstrated that opioids modulate the renin-angiotensin and sympathetic nervous systems. To clarify the interaction of central angiotensin II (Ang II) and endogenous opioids, we studied the effects of naloxone, an opioid antagonist, on cardiovascular and sympathetic responses to intracerebroventricular (ICY) Ang II in conscious rabbits. ICV Ang II (20 ng/min) significantly increased mean arterial pressure (MAP), plasma epinephrine, and arginine vasopressin (AVP) levels, with no significant change in renal sympathetic nerve activity (RSNA) or heart rate. Pretreatment with intravenous naloxone (0.1 mg/kg) failed to alter the cardiovascular and neurohormonal responses to ICY Ang II. To eliminate the effect of AVP on cardiovascular and sympathetic responses, [d(CH2)5Thy(Me)]AVP, a vasopressin V1-receptor antagonist, was given intravenously. Pretreatment with intravenous injection of the V1-receptor antagonist (30 pg/kg) augmented the maximum increase in RSNA caused by ICV Ang II (8.9 ± 2.2 vs. 16.2 ± 0.7% , p < 0.05). Combined pretreatment with naloxone and V1-receptor antagonist further increased MAP and RSNA in response to ICY Ang II (20 ± 1 vs. 16 ± 2 mmHg, p < 0.05, and 30.9 ± 3.7 vs. 16.2 ± 0.7% , p < 0.01, respectively). These results suggest that opioids and AVP synergistically modulate sympathetic outflow so as to suppress the central pressor action of Ang II in conscious rabbits. (Hypertens Res 1998; 21: 89-95)

Central effects of leptin on cardiovascular and neurohormonal responses in conscious rabbits

“…It seems difficult to interpret the time course difference between the present study and the previous ones; however, it may be explained by the experimental design, such as dose of leptin, route of administration, the species used in the experiments, and the state of consciousness of the animals. Rabbits may be resistant to increase arterial pressure compared with rats, because even intracerebroventricular infusion of angiotensin II caused only a small increase in MAP in conscious rabbits (7). The present study did not provide the mechanisms of pressor response and activation of sympathetic nervous system induced by intracerebroventricular leptin.…”

Shedding Light on the Pharmacological Interactions between μ-Opioid Analgesics and Angiotensin Receptor Modulators: A New Option for Treating Chronic Pain

“…This does not necessarily mean that there are no possible interactions between the two systems. Indeed, there are several reports, indicating opioids are capable of changing physiological parameters, most notably changes in the blood pressure [144][145][146][147][148] or drinking-response to AngII [149][150][151]. However, regarding the relationship between RAS and the opioid system only a small proportion of these address the role of interactions in analgesia.…”

Augmented myocardial methionine-enkephalin in a murine model of cardiac angiotensin II-overexpression

“…[15][16][17]27 The level of sympathetic activation in the TG1306/1R has not been specifically examined, but it is possible that the late rise in cardiac ME in these mice represents a compensatory response to curb Ang II-induced catecholamine effects. However, given that the heart rate is not elevated in the transgenic mice 22 implying undisturbed basal autonomic function, an alternative possibility is of a non-sympathetic dependent, local enkephalin action.…”

“…activation of the sympathetic nervous system may also provoke a hypertrophic response through an increase in catecholamine release. [15][16][17]27 The level of sympathetic activation in the TG1306/1R has not been specifically examined, but it is possible that the late rise in cardiac ME in these mice represents a compensatory response to curb Ang II-induced catecholamine effects. However, given that the heart rate is not elevated in the transgenic mice 22 33 have demonstrated that there is a reduced responsiveness to OPR agonists and reduced OPR-mediated cardioprotection against ischaemia-reperfusion injury in senescent hearts.…”

“…The endogenous opioid system has also (albeit less extensively) been reported to interact with the RAS and exert an inhibitory effect on Ang II. [15][16][17] Fukuhara et al, 15 found that opioids and arginine vasopressin synergistically modulate sympathetic outflow and thus suppress the central pressor action of Ang II in the conscious rabbit. Ang II is known to stimulate the release of norepinephrine and epinephrine from the adrenal glands and sympathetic nerve endings.…”