Effect of naloxone on baroreflex, sympathetic tone and blood pressure in the cat

Koyama, Shozo; Manugian, Vivian; Ammons, W. S.; Santiesteban, Hector; Manning, Janet R.

doi:10.1016/0014-2999(83)90558-7

Cited by 29 publications

(7 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Twenty-one subjects (19 men and two women aged 24+1 [mean±SEM] years) were studied in three treatment groups: 0.15 mg/kg naloxone (n=14, subjects 1-14), 0.075 mg/kg naloxone (n=13, subjects 9-21), and placebo (n=11, subjects [4][5][6][7][8][9][10][11][12][13][14]. Thus, six subjects (subjects 9-14) were studied with both doses of naloxone, and all but three subjects in the higher dose naloxone group were also studied after placebo.…”

Section: Subjects and Methods Subjectsmentioning

confidence: 99%

“…The hemodynamic and MSNA responses of subjects during application of incremental LBNP (0, -5, -10, and -15 mm Hg) before and after administration of 0.15 mg/kg naloxone (subjects [1][2][3][4][5][6][7][8][9][10][11][12][13][14] and 0.075 mg/kg naloxone (subjects 9-21) are summarized in Tables 1 and 2 and Figures 1 and 2.…”

Section: Effects Ofnaloxone On Responses To Cardiopulmonarymentioning

confidence: 99%

“…[7][8][9][10][11][12] In humans, the arterial baroreflex control of heart rate during arterial baroreceptor deactivation with nitroprusside is potentiated by naloxone.13 Deactivation of cardiopulmonary baroreceptors during nonhypotensive hemorrhage has been shown to increase the secretion of adrenocorticotropic hormone (ACTH) in animals. '4"15 ,3-Endorphins, which have high affinity for ,u opioid receptors, are known to be released concomitantly and in equimolar concentrations with ACTH from the pituitary.…”

mentioning

confidence: 99%

See 2 more Smart Citations

Naloxone potentiates cardiopulmonary baroreflex sympathetic control in normal humans.

Schobel

Oren

Mark

et al. 1992

Circulation Research

View full text Add to dashboard Cite

Naloxone, an opioid antagonist, augments baroreflex mechanisms in animals; this occurrence suggests that endogenous opioids blunt baroreflex responses. Limited human studies suggest an inhibitory action of endogenous opioids on baroreflex-mediated vagal responses during arterial baroreceptor deactivation. To evaluate the potential effect of endogenous opioids on cardiopulmonary baroreflex mechanisms in humans, we measured arterial and central venous pressures, heart rate, and efferent muscle sympathetic nerve activity (MSNA, by peroneal microneurography) during unloading of cardiopulmonary baroreceptors with incremental lower body negative pressure (LBNP, from 0 to -15 mm Hg) and during the cold pressor test in 21 normal subjects (aged 24±1 [mean±SEM] years). In 14 subjects, we performed LBNP before and after naloxone (0.15 mg/kg i.v.) and placebo (n = 11) on separate days. In six of these 14 subjects and an additional seven subjects (n=13), studies were also performed before and after administration of a lower dose of naloxone (0.075 mg/kg i.v.) on separate days. Neither dose of naloxone significantly altered control arterial or central venous pressures or heart rate. Control MSNA was reduced after the higher but not after the lower dose of naloxone. Comparable reductions in central venous pressure were produced by LBNP in all groups before and after naloxone or placebo, whereas LBNP did not alter arterial pressure. Cardiopulmonary baroreflex sympathetic sensitivity, which was derived as the slope of the linear regression relation between percent change in total MSNA (units) per absolute change in central venous pressure (mm Hg) during incremental LBNP, was significantly augmented after both the high dose (from 18.6±4.7%o/mm Hg to 39.3±8.1%o/mm Hg, p=0.001) and low dose of naloxone, whereas placebo had no effect. MSNA responses to the cold pressor test were not altered by (1987)(1988)(1989)(1990) where baroreceptor and chemoreceptor afferents terminate, there has been increasing interest in the possibility that endogenous opioids are involved in the physiological regulation of baroreflex mecha-

show abstract

Section: Subjects and Methods Subjectsmentioning

confidence: 99%

Section: Effects Ofnaloxone On Responses To Cardiopulmonarymentioning

confidence: 99%

mentioning

confidence: 99%

See 1 more Smart Citation

Naloxone potentiates cardiopulmonary baroreflex sympathetic control in normal humans.

Schobel

Oren

Mark

et al. 1992

Circulation Research

View full text Add to dashboard Cite

show abstract

“…These peptides were shown to affect the brainstem (FLORETZ and MEDIAVILLA, 1977) and to modify the baroreceptor reflex at the level of the nucleus tractus solitalius (BOLME et al, 1978;SCHAZ et al, 1980;YUKIMURA et al, 1981;PETTY and DE JONG, 1982). Additionally, both intravenously and intracisternally injected naloxone, specific opiate antagonist, caused a facilitation of carotid sinus baroreflex in anesthetized cat (KOYAMA et a!., 1983a). Naloxone reversed the systemic hypotension and depressed sympathetic activity induced by E. coli endotoxin (KOYAMA et a!., 1983b).…”

mentioning

confidence: 99%

No evidence of direct cardiac action of leucine-enkephalin in canine heart-lung preparation.

et al. 1984

Self Cite

View full text Add to dashboard Cite

Summary Intravenous administration of leucine-enkephalin (30 pg/kg) caused significant decreases in mean blood pressure, cardiac output, and left ventricular dP/dt in intact dogs. However, cardiovascular effects of leucine-enkephalin (30-120 µg/kg) did not occur in the heartlung preparation uninfluenced by extracardiopulmonary factors. These results provide no evidence of a direct cardiac action of leucine-enkephalin.

show abstract

“…21 However, in anesthetized cats, intravenous injection of naloxone (2.0 mg/kg) produced significant increases in mean arterial pressure, pulse pressure, and preganglionic splanchnic nerve activity. 22 Thus, under anesthetized or acute surgical conditions, hemodynamics and the autonomic nervous system are already modified by endogenous opiate peptides. These differences may contribute to the difference between conscious and anesthetized animals in response of the autonomic nervous system to hemorrhage.…”

Section: Original Record Illustrating Responses Of Arterial Pressurmentioning

confidence: 99%

Opiate receptor-mediated decrease in renal nerve activity during hypotensive hemorrhage in conscious rabbits.

Morita

Nishida

Motochigawa

et al. 1988

Circulation Research

View full text Add to dashboard Cite

Effects of hemorrhage on renal nerve activity and of subsequent opiate receptor blockade with naloxone were studied in conscious rabbits. Mean arterial pressure remained constant at 77 ± 2 mm Hg through 17 ±2 ml/kg hemorrhage, while renal nerve activity increased by 159±16%. After 25 ± 1 ml/kg hemorrhage, mean arterial pressure fell by 42 ± 3 mm Hg, and renal nerve activity decreased below the prehemorrhagic control level by 41 ±15%. Bolus injection of naloxone (3 mg/kg i.v.) increased mean arterial pressure to 79 ±2 mm Hg, not significantly different from the prehemorrhagic control level. Renal nerve activity increased by 171 ±28%, comparable to the peak increase during nonhypotensive hemorrhage. On a different day, hemorrhage was repeated, and phenylephrine was infused during the subsequent hypotension. Phenylephrine increased mean arterial pressure to the prehemorrhagic control level. With increasing mean arterial pressure, renal nerve activity increased from its level during hypotensive hemorrhage and recovered toward the prehemorrhagic control level ( -26±11%), but it did not return to the peak value reached during nonhypotensive hemorrhage. To further examine the blocking effects of naloxone on changes in mean arterial pressure and renal nerve activity induced by exogenous opiate peptides, methionine-enkephalin was injected both in the control state and after treatment with naloxone. A bolus injection of methionine-enkephalin (10 fig/kg) decreased mean arterial pressure ( -8.1 ±2.0 mm Hg) and renal nerve activity ( -95 ± 1%). Pretreatment with naloxone (0.5 mg/kg) effectively blocked this depressor effect and reduction in renal nerve activity. These results indicate that hi conscious rabbits, hemorrhage elicits a biphasic effect on renal nerve activity that rises initially during nonhypotensive hemorrhage and then falls during hypotensive hemorrhage. This decrease in renal nerve activity is reversed by naloxone. Therefore, one mechanism by which renal nerve activity decreases during hypotensive hemorrhage appears to involve opiate receptors.

show abstract

Effect of naloxone on baroreflex, sympathetic tone and blood pressure in the cat

Cited by 29 publications

References 23 publications

Naloxone potentiates cardiopulmonary baroreflex sympathetic control in normal humans.

Naloxone potentiates cardiopulmonary baroreflex sympathetic control in normal humans.

No evidence of direct cardiac action of leucine-enkephalin in canine heart-lung preparation.

Opiate receptor-mediated decrease in renal nerve activity during hypotensive hemorrhage in conscious rabbits.

Contact Info

Product

Resources

About