Structure-activity evidence against opiate receptor involvement in Leu5-enkephalin- induced pulmonary vasoconstriction

Crooks, Peter A.; Bowdy, Bruce D.; Reinsel, Carol N.; Iwamoto, Edgar T.; Gillespie, Mark N.

doi:10.1016/0006-2952(84)90028-5

Cited by 6 publications

(2 citation statements)

References 15 publications

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“…20 action, was not reversed by naloxone. Nor was such reversal seen in the case of vasoconstrictor action of [Leu 5 ]enkephalin] (Crooks et al 1984).…”

Section: Paradoxical Increases In Map After Biphalinmentioning

confidence: 91%

“…Remarkably, another enkephalin analogue, [Leu 5 ]enkephalin was also reported to cause vasoconstriction and blood pressure increase (Crooks et al 1984;Giles and Sander 1983). While opioids can directly stimulate brain centres leading to enhancement of sympathetic output and to peripheral vasoconstriction (Bali at al.…”

Section: Paradoxical Increases In Map After Biphalinmentioning

confidence: 97%

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Different blood pressure responses to opioids in 3 rat hypertension models: role of the baseline status of sympathetic and renin–angiotensin systems

Bądzyńska

Lipkowski

Olszyński

et al. 2016

Can. J. Physiol. Pharmacol.

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Opioids interact with sympathetic and renin-angiotensin systems in control of mean arterial pressure (MAP). Our earlier finding that biphalin, a synthetic enkephalin analogue, decreased MAP in anaesthetized spontaneously hypertensive rats (SHR) prompted us to further explore this action, to get new insights into pathogenesis of various forms of hypertension. Biphalin effects were studied in SHR, uninephrectomized rats on a high-salt diet (HS/UNX), and rats with angiotensin-induced hypertension (Ang-iH). Besides MAP, renal and iliac blood flows (RBF, IBF) and vascular resistances were measured. In anaesthetized and conscious SHR, biphalin (300 μg·h·kg i.v.) decreased MAP by ∼10 and ∼20 mm Hg, respectively (P < 0.001). In anaesthetized HS/UNX and normotensive rats, MAP increased by ∼6-7 mm Hg (P < 0.02); without anaesthesia, only transient decreases occurred. MAP never changed in Ang-iH rats. Morphine (1.5 mg·h·kg i.v.) decreased MAP in HS/UNX but only transiently so without anaesthesia; such anaesthesia dependence of response was also seen in normotensive rats. Ang-iH rats never responded to morphine. Hypotensive effect in SHR only depends primarily on the reduction by biphalin of vascular responsiveness to increased sympathetic stimulation; such increase is well documented for SHR. No MAP response to biphalin or morphine in Ang-iH could depend on angiotensin-induced alterations of the vascular wall morphology and function.

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“…20 action, was not reversed by naloxone. Nor was such reversal seen in the case of vasoconstrictor action of [Leu 5 ]enkephalin] (Crooks et al 1984).…”

Section: Paradoxical Increases In Map After Biphalinmentioning

confidence: 91%