Influence of chronic naloxone treatment on development of hypertension in the spontaneously hypertensive rat

Quock, Raymond M.; Vaughn, Linda K.; Kouchich, F. J.

doi:10.1007/bf00507060

Cited by 28 publications

(7 citation statements)

References 18 publications

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“…49 - 12 In part, this may be due to the possibility that endogenous opioid systems remain silent until activated by specific stimuli. In this manner, the arterial hypotension of endotoxic, circulatory, and hemorrhagic shock have been shown to be antagonized by blockade of opioid receptors with naloxone.…”

Section: Discussionmentioning

confidence: 99%

Opioids in the systemic hemodynamic and renal responses to stress in spontaneously hypertensive rats.

1989

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Endogenous opioid peptides have been implicated in the regulation of cardiovascular and renal function. We tested this hypothesis by examining whether the opioid antagonist naloxone alters the cardiovascular or renal responses produced by environmental stress (air stress) in conscious spontaneously hypertensive rats (SHR). Before naloxone administration, air stress produced significant increases in heart rate, mean arterial pressure, and renal sympathetic nerve activity, and it caused a decrease in urinary sodium excretion. After intravenous and intracerebroventricular administration of naloxone, the air stress-induced pressor and antinatriuretic responses were inhibited. Subsequent studies with a different opioid antagonist, the quaternary compound naltrexone methylbromide, also showed inhibition of the air stress-induced pressor and antinatriuretic responses and demonstrated opioid receptor specificity of this inhibition. Furthermore, since only intracerebroventricular and not intravenous administration of naltrexone methylbromide inhibited the pressor and antinatriuretic responses to air stress, a central nervous system site of action was established. The opioid antagonists caused inhibition of the pressor and antinatriuretic responses to air stress without affecting the air stress-induced increase in renal sympathetic nerve activity. Our investigations indicate that central endogenous opioid peptides contribute to the pressor and antinatriuretic responses that occur in conscious SHR during acute environmental stress. {Hypertension 1989; 13:808-816)

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Section: Discussionmentioning

confidence: 99%

Opioids in the systemic hemodynamic and renal responses to stress in spontaneously hypertensive rats.

1989

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“…Regulatory Systems An interesting question regarding pain and cardiovascular regulatory systems relates to the functional organization that supports this interaction. At least two schemes based on existing anatomical, physiological, and behavioral evidence (Randich and Maixner, 1984[a]; Smith and DeVito, 1984;Janig, 1985;Randich and Aicher, 1988;Loewy, 1990) can be proposed. Tbe first scheme is based on that predicted by Cannon's (1927Cannon's ( , 1939 thalamic theory of emotions.…”

Section: Organizational Schemes Supporting An Interaction Between Carmentioning

confidence: 99%

Interactions Between Cardiovascular and Pain Modulatory Systems: Physiological and Pathophysiological Implications

Maixner

1991

Cardiovasc electrophysiol

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Cardiovascular and Pain Regulatory Systems. Several recent findings provide evidence that cardiovascular and pain regulatory systems are interactive. Tbe physiological responses to acute pain are discussed and hypothetical organizational models that explain how cardiovascular and pain regulatory systems interact are proposed. The adaptive value of interactions between cardiovascular and pain regulatory systems is discussed. It is proposed that maladaptive cardiovascular-somatosensory interactions may contribute to several cardiovascular disorders sucb as essential hypertension, asymptomatic myocardial ischemia, and life-threatening cardiac arrhythmias. (

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“…In general, in experimental studies brain opioid systems were reported to exert hypertensive or hypotensive influence via stimulation or inhibition of central sympathetic output, the effect depending on the actual brain structures and the opioid receptor species involved (Appel et al 1986;Siren and Feuerstein 1992). For instance, one early study suggested that enhancement by morphine of Ang II dependent pressor effects was mediated by stimulation of circumventricular organs (probably area postrema) (Shilagyi and Ferrario 1981), and chronic inhibition of opioid receptors with naloxone was reported to suppress the development of hypertension in young SHR (Quock et al 1984). On the other hand, other workers did not find convincing evidence on the role of brain opioid systems in experimental hypertension (Sun et al 1996).…”

Section: Introductionmentioning

confidence: 97%

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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Influence of chronic naloxone treatment on development of hypertension in the spontaneously hypertensive rat

Cited by 28 publications

References 18 publications

Opioids in the systemic hemodynamic and renal responses to stress in spontaneously hypertensive rats.

Opioids in the systemic hemodynamic and renal responses to stress in spontaneously hypertensive rats.

Interactions Between Cardiovascular and Pain Modulatory Systems: Physiological and Pathophysiological Implications

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

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