A Computer for the Calculation of Skeletal Muscle Vascular Resistance

Zambuto, Raymond Peter; Reder, Ronald E.; Sanders, Charles A.; Powell, Wilson M.

doi:10.1109/tbme.1972.324091

Cited by 1 publication

(1 citation statement)

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“…The left gracilis muscle was removed prior to the experiment, and its weight was used in the resistance calculation since the right and left • gracilis muscles are of equal weight. 28 …”

Section: Experimental Preparationmentioning

confidence: 99%

Neurogenic histaminergic vasodilation in canine skeletal muscle: mediation by alpha 2-adrenoceptor stimulation.

Camazine

Shannon

Guerrero

et al. 1988

Circulation Research

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This study examines the neurogenic effect of a 2 -adrenoceptor stimulation on skeletal muscle vascular resistance and its relation to the level of background sympathetic activity. The isolated, separately perfused, neurally intact canine gracilis muscle preparation was used since it permits deliberate and quantifiable alterations in background sympathetic activity, as measured by skeletal muscle vascular resistance. Systemic intravenous UK-14304, a highly selective a,-adrenoceptor agonist, produced a precipitous, neurogenic vasodilation that lowered vascular resistance below the subsequently denervated resistance, thus indicating that an active vasodilation was involved. The overall magnitude of the vasodilation was much greater in animals that had been hemorrhaged to elevate background sympathetic activity than in animals that had been transfused to lower background activity. The 4 " 7 The vascular response to stimulation of the o^-adrenoceptor depends on its junctional location; postjunctionalry, this receptor mediates vasoconstriction while prejunctionalry, it mediates vasodilation.8 "" Thus, the net effect of an Oj-adrenoceptor agonist reflects the balance between its postjunctional vasoconstrictor effect and its prejunctional vasodilator effect.Centrally located o^-adrenoceptors, in particular, appear to play a crucial role in the regulation of the cardiovascular system. Stimulation of these receptors inhibits sympathetic neurotransmission and produces a fall in blood pressure.12 As a result, this receptor has been the target of an increasing number of receptorspecific agents to treat hypertension. Clonidine and the more selective c^-adrenoceptor agonists UK-14304 and B-HT 920 are the most potent centrally acting

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“…The left gracilis muscle was removed prior to the experiment, and its weight was used in the resistance calculation since the right and left • gracilis muscles are of equal weight. 28 …”

Section: Experimental Preparationmentioning

confidence: 99%