Some cardiovascular effects of ST-91 and clonidine

Scriabine, Alexander; Sweet, Charles S.; Ludden, C. T.; Stavorski, John M.; Wenger, Herbert C.; Bohidar, N. R.

doi:10.1016/0014-2999(77)90039-5

Cited by 35 publications

(9 citation statements)

References 13 publications

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“…prazosin) drugs (Langer, 1974b(Langer, , 1976Stjarne, 1975;Stake, 1977;Westfall, 1977;Bevan, 1978;Langer, Starke & Dubocovich, 1979;Lorenz, Vanhoutte & Shepherd, 1979). Although clonidine has a great affinity for peripheral prejunctional a-adrenoreceptors, it is unlikely that this effect contributes to its antihypertensive effect (Haeusler, 1974(Haeusler, , 1976Scriabine, Sweet, Ludden, Stavorski, Wenger & Bohidar, 1977). The low affinity of prazosin for prejunctional a-adrenoreceptors helps to explain why the compound, unlike most other a-adrenolytic agents, does not induce tachycardia (Cambridge, Davey & Massingham, 1977: Lefevre-Borg, Roach & Cavero, 1979.…”

Section: Prejunctional Inhibition A-adrenoreceptor Feedback Inhibitionmentioning

confidence: 95%

Pre- and Post-Junctional Adrenergic Mechanisms and Hypertension

1980

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1. The ability of the blood vessel wall to synthesize noradrenaline is augmented at the early stages of genetic hypertension in animals. It usually is normal, or reduced in chronic hypertension. 2. The exocytotic release of noradrenaline is greater than normal, in the early stages of a number of experimental models of hypertension. 3. Postjunctional receptors for noradrenaline are not uniform throughout the vascular tree. Their sensitivity changes during the development of high blood pressure. 4. In chronic hypertension neuronal uptake and the extraneuronal disposition of released noradrenaline is depressed in the heart, but accelerated in the blood vessel wall. 5. The adrenergic neuro-effector interaction undergoes a diverging long-term adaptation in the heart and the blood vessels of hypertensive animals. In the former this tends to increase, but in the latter to reduce, the efficiency of sympathetic nervous control.

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Section: Prejunctional Inhibition A-adrenoreceptor Feedback Inhibitionmentioning

confidence: 95%

Pre- and Post-Junctional Adrenergic Mechanisms and Hypertension

1980

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“…Ventricular injections of clonidine mimic the inhibitory effect of the drug’s systemic injections (Shaham et al 2000b), while systemic injections of ST-91, a charged analogue of clonidine that does not readily cross the blood–brain barrier (Scriabine et al 1975), had no effect on footshock-induced reinstatement. Another finding from this series of studies is that systemic injections of the alpha-2 adrenoceptor agonists had no effect on reinstatement of drug seeking induced by drug priming injections or exposure to drug-associated cues (Erb et al 2000; Highfield et al 2001).…”

Section: Effect Of Alpha-2 Adrenoceptor Agonists On Stress-induced Rementioning

confidence: 99%

Translational and reverse translational research on the role of stress in drug craving and relapse

2011

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Rationale and background High relapse rates during abstinence are a pervasive problem in drug addiction treatment. Relapse is often associated with stress exposure, which can provoke a subjective state of drug craving that can also be demonstrated under controlled laboratory conditions. Stress-induced relapse and craving in humans can be modeled in mice, rats, and monkeys using a reinstatement model in which drug-taking behaviors are extinguished and then reinstated by acute exposure to certain stressors. Studies using the reinstatement model in rats have identified the role of several neurotransmitters and brain sites in stress-induced reinstatement of drug seeking, but the degree to which these preclinical findings are relevant to the human condition is largely unknown. Objectives and highlights Here, we address this topic by discussing recent results on the effect of alpha-2 adreno-ceptors and substance P-NK1 receptor antagonists on stress-induced reinstatement in mice and rats and stress-induced craving and potentially stress-induced relapse in humans. We also discuss brain sites and circuits involved in stress-induced reinstatement of drug seeking in rats and those activated during stress-induced craving in humans. Conclusions There is evidence that alpha-2 adrenoceptor agonists and NK1 receptor antagonists decrease stress-induced drug seeking in rats and stress-induced craving in humans. Whether these drugs would also prevent stress-induced drug relapse in humans and whether similar or different brain mechanisms are involved in stress-induced reinstatement in non-humans and stress-induced drug craving and relapse in humans are subjects for future research.

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“…Further, it has been noted that, unlike clonidine, ST-91 evokes minimal sedation. These differences were largely attributed to physicochemical and pharmacokinetic parameters (Hoefke et al, 1975; Scriabine et al, 1977). Yaksh and Reddy later showed for the first time that intrathecally delivered ST-91 evoked antinociceptive responses in macaque (Yaksh & Reddy, 1981) when delivered alone and in combination with morphine.…”

Section: 7 St91mentioning

confidence: 99%

Pharmacological profiles of alpha 2 adrenergic receptor agonists identified using genetically altered mice and isobolographic analysis

Fairbanks

Stone

Wilcox

2009

Pharmacology & Therapeutics

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Endogenous, descending noradrenergic fibers convey powerful analgesic control over spinal afferent circuitry mediating the rostrad transmission of pain signals. These fibers target alpha 2 adrenergic receptors (α 2 ARs) on both primary afferent terminals and secondary neurons, and their activation mediates substantial inhibitory control over this transmission, rivaling that of opioid receptors which share similar a similar pattern of distribution. The terminals of primary afferent nociceptive neurons and secondary spinal dorsal horn neurons express α 2A AR and α 2C AR subtypes, respectively. Spinal delivery of these agents serves to reduce their side effects, which are mediated largely at supraspinal sites, by concentrating the drugs at the spinal level. Targeting these spinal α 2 ARs with one of five selective therapeutic agonists, clonidine, dexmedetomidine, brimonidine, ST91 and moxonidine, produces significant antinociception that can work in concert with opioid agonists to yield synergistic antinociception. Application of several genetically altered mouse lines had facilitated identification of the primary receptor subtypes that likely mediate the antinociceptive effects of these agents. This review provides first an anatomical description of the localization of the three subtypes in the central nervous system, second a detailed account of the pharmacological history of each of these six primary agonists, and finally a comprehensive report of the specific interactions of other GPCR agonists with each of the six principal α 2 AR agonists featured.

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Some cardiovascular effects of ST-91 and clonidine

Cited by 35 publications

References 13 publications

Pre- and Post-Junctional Adrenergic Mechanisms and Hypertension

Pre- and Post-Junctional Adrenergic Mechanisms and Hypertension

Translational and reverse translational research on the role of stress in drug craving and relapse

Pharmacological profiles of alpha 2 adrenergic receptor agonists identified using genetically altered mice and isobolographic analysis

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