Enhanced presynaptic beta 2-adrenergic facilitatory mechanism in conscious deoxycorticosterone acetate-salt hypertensive rats.
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Animals↗
Biomedical subjects
J de Champlain
Publications and source records attributed to J de Champlain.
Chronic effects of diltiazem on the hemodynamic and sympathoadrenal tone in responsive and nonresponsive hypertensive patients at rest and during isometric exercise.
The objective of this study was to identify hemodynamic and sympathetic parameters that could be predictive of the hypotensive response to diltiazem (DTZ). Parameters of cardiovascular functions were measured from M-mode echocardiography and the index of sympathoadrenal tone was given by circulating catecholamine levels in 25 normotensive subjects and in 19 mild-to-moderate hypertensive patients before and after 2 months as well as 12 months (responders only) of treatment with DTZ (SR 120 or 180 mg b.i.d.). The responder (R) subgroup (63% of total population) consisted of patients who showed a decrease in mean arterial pressure (MAP) greater than or equal to 5 mm Hg (day average) by ambulatory blood pressure (BP) monitoring. Before treatment, R patients were characterized by higher circulating norepinephrine (NE) levels and by hyperkinetic cardiac functions [increased heart rate (HR), cardiac index (CI), and mean velocity of circumferential fiber shortening, p less than 0.05] while peripheral resistance was normal. In contrast, nonresponders (NR) were characterized by higher peripheral resistance (p less than 0.05) and normal cardiac functions. Following treatment, hyperkinetic cardiac functions were normalized but the peripheral resistance was unchanged in the R subgroup whereas in the NR subgroup, cardiac parameters were slightly increased and the peripheral resistance was normalized. During isometric exercise, cardiac performance was found to be impaired (p less than 0.05) and the increase in peripheral resistance was greater (p less than 0.05) in the R subgroup before treatment, whereas those responses were normal in the BR group.(ABSTRACT TRUNCATED AT 250 WORDS)
Adrenal Glands↗
Recommendations of the Canadian Consensus Conference on Non-Pharmacological Approaches to the Management of High Blood Pressure, Mar. 21-23, 1989, Halifax, Nova Scotia.
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Adult↗
Alpha 2-adrenoceptor modulation of catecholamine and neuropeptide Y responses during haemorrhagic hypotension in anaesthetized dogs.
The acute effects of oxymetazoline, an alpha 2-adrenoceptor agonist, and idazoxan, an alpha 2-adrenoceptor antagonist, on the release of neuropeptide Y were evaluated during haemorrhage in pentobarbital-anaesthetized dogs. Plasma concentrations of neuropeptide Y and catecholamines (adrenaline, noradrenaline, and dopamine) were determined in samples simultaneously collected from aorta, portal vein, and adrenal veins. In control dogs, adrenal catecholamine output, aortic concentrations neuropeptide Y and catecholamines markedly increased during the hypotension period. However, adrenal neuropeptide Y output decreased significantly during this period. Portal venous noradrenaline and neuropeptide Y concentrations increased significantly. In dogs treated with idazoxan, catecholamine output from the adrenals increased to an extent similar to that observed in control dogs. However, the increase in noradrenaline and neuropeptide Y in aortic or portal venous blood during haemorrhage was significantly potentiated in the presence of idazoxan. Administration of oxymetazoline abolished this increase, but did not alter adrenal catecholamine or neuropeptide Y output. The present study demonstrates that neuropeptide Y is co-released with noradrenaline from sympathetic nerve fibers during haemorrhage. Since the release of neuropeptide Y appeared to follow a similar time course to that of noradrenaline release, the present observations suggest that haemorrhagic hypotension enhances both neuropeptide Y and noradrenaline release presumably through a common releasing mechanism. These results also indicate that, in peripheral sympathetic nerves but not in the adrenal gland, neuropeptide Y release is also modulated presynaptically by the inhibitory alpha 2-adrenoceptors in conjunction with the noradrenaline release.
Adrenergic alpha-Antagonists↗
Chronic doxorubicin induced cardiomyopathy in rabbits: mechanical, intracellular action potential, and beta adrenergic characteristics of the failing myocardium.
STUDY OBJECTIVE: The aim was to assess myocardial, electrophysiological, and adrenergic changes caused by chronic administration of doxorubicin. DESIGN: Doxorubicin induced cardiotoxicity was produced in three groups of rabbits by injecting doxorubicin 0.75 mg.kg-1 three times a week for 7, 9 and 11 weeks. There were 36 controls. All studies were conducted within 16 to 36 h after the last injection. Histological, mechanical, and action potential changes produced by doxorubicin were examined in vitro. The effects of doxorubicin on beta adrenergic receptors and cyclic adenosine monophosphate (AMP) generation in myocardial membrane preparations were also evaluated. EXPERIMENTAL MATERIAL: 145 New Zealand white rabbits, 2.4-2.7 kg, were used. After excision of the heart, a papillary muscle was used for mechanical studies, a portion of the septum for intracellular action potential studies, and the rest of the heart for histological or biochemical studies. MEASUREMENTS AND RESULTS: Histological studies showed widespread myocardial damage that became more severe as the cumulative doses increased. Right ventricular papillary muscles of doxorubicin treated rabbits had lower total tension (1.5 v 3.3 g.mm-2 for controls, p less than 0.05) and dT/dt, shorter contraction duration, and lower velocity of shortening than the control muscles under all loading conditions. The changes progressed as the cumulative doxorubicin dose increased. Action potential duration was shorter in the doxorubicin treated groups (APD50 = 76 v 62 ms for controls, p less than 0.01), although resting action potential amplitude was normal. Tension-frequency response (6-36 stimuli.min-1) and response to increasing calcium concentrations (2.54-6.32 mM) were attenuated in the doxorubicin group. Percent change in tension and dT/dt in response to noradrenaline (50 microM), isoprenaline (20 microM), or dibutyryl cyclic AMP (40 mM), was increased in the doxorubicin group v controls (300-600% v 100-200% respectively), despite chronic increase in circulating catecholamines, depletion of myocardial catecholamines, and no change in beta adrenergic receptor number or affinity. The apparent increase in beta adrenergic responsiveness in the doxorubicin group may have been partly due to decreased basal cyclic AMP production (13 v 31 pMol.mg-1 protein.min-1, p less than 0.01), although maximum catecholamine stimulated cyclic AMP production was only mildly decreased (251 v 315 pMol.mg-1 protein.min-1, p less than 0.05). CONCLUSIONS - The subacute effects of chronic doxorubicin become progressively more marked as the cumulative dose increases, and there are significant differences in the myocardial characteristics between this chronic model and other models of heart failure. These differences may be related to the cytotoxic effects of doxorubicin on membranes and membrane bound enzymes.
Action Potentials↗
Occlusion time dependency of regional noradrenaline release and cardiac arrhythmias during reperfusion of acutely ischaemic heart in the dog in vivo.
STUDY OBJECTIVE: The aim was to study the occlusion time dependency of reperfusion induced increases in regional cardiac noradrenaline release from the ischaemic area in relation to the incidence of ventricular arrhythmias. DESIGN: The left anterior descending coronary artery was ligated for 15, 30 and 60 min in three separate groups of dogs (n = 10 per group). Each occlusion period was followed by a 30 min reperfusion period. The coronary sinus and the epicardial vein running in parallel with the left anterior descending coronary artery were cannulated for measurement of noradrenaline and lactate. EXPERIMENTAL MATERIAL: 30 adult mongrel dogs, 22.5(SEM 1.1) kg, were used for the study. The animals were anaesthetised with sodium pentobarbitone. MEASUREMENTS AND MAIN RESULTS: During occlusion, epicardial venous blood noradrenaline concentrations remained unchanged up to 30 min, but increased from 0.133(0.027) ng.ml-1 to 0.289(0.069) ng.ml-1 after 60 min of occlusion (p less than 0.05). However, epicardial venous blood lactate concentrations increased immediately upon occlusion, and remained elevated (p less than 0.05) during the whole period of occlusion in all groups. Neither noradrenaline nor lactate concentrations in coronary sinus blood increased during occlusion. During reperfusion, nine dogs showed early ventricular fibrillation. The highest incidence of fibrillation (n = 5/10) was found in the 15 min occlusion group, but the difference was not significant between groups. Epicardial venous blood noradrenaline concentrations increased to 0.371(0.076) ng.ml-1, 0.470(0.178) ng.ml-1, and 1.824(0.713) ng.ml-1 upon reperfusion following 15, 30 and 60 min occlusion, respectively (each p less than 0.05). Maximum increases in epicardial venous blood noradrenaline concentrations during reperfusion were correlated with duration of preceding occlusion (r = 0.60, n = 21, p less than 0.01). Maximum increases in mean arrhythmic ratios observed during the first 10 min of reperfusion were proportionally related to mean epicardial venous blood noradrenaline concentrations. The increases in epicardial venous blood noradrenaline concentrations and the incidence of ventricular arrhythmias in the 60 min occlusion group were greater (p less than 0.05) than in the other two groups. CONCLUSIONS: This study shows that noradrenaline is released progressively from the ischaemic area during occlusion for 60 min. The amount of noradrenaline washed out upon reperfusion and the incidence of reperfusion ventricular arrhythmias both appear to be dependent upon duration of preceding occlusion. The results suggest that cardiac noradrenaline released locally from the ischaemic region may contribute to the genesis of reperfusion ventricular arrhythmias, but not to that of reperfusion ventricular fibrillation.
Animals↗
Sympathoadrenal mechanisms underlying cardiovascular responses to intrathecal substance P in conscious rats.
The sympathoadrenal mechanisms underlying cardiovascular responses to intrathecal (i.th.) injection of substance P (SP), at the T-9 spinal level, were investigated in conscious rats. Release of norepinephrine (NE), and epinephrine (EPI) could be induced by 6.5, 16.25, and 32.5 nmol SP correlated with a pressor and a positive chronotropic response. Release of neuropeptide Y (NPY) was evoked also by 32.5 nmol SP, and released NPY appears to derive from the adrenal medulla. The initial pressor response in intact rats is mediated by NE from sympathetic fibers, whereas the latent pressor response, observed in sympathectomized rats, is possibly due to NPY from the adrenal medulla. Although a functional balance between the sympathetic fibers and the adrenal glands is supported by the results, it appears that only the tachycardia can be efficiently produced by the adrenals in the absence of the sympathetic fibers. This study supports a functional role for SP in regulation of the sympathoadrenal system at the spinal level.
Adrenal Medulla↗
Absence of prejunctional sympathetic effect of amiodarone in hearts of open-chest anesthetized dogs.
The effect of amiodarone (30 mg/kg p.o. each day for 3 weeks) on noradrenaline (NA) overflow into coronary sinus (CS) blood during left stellate stimulation (15 V, 2-ms square waves, 30 s duration at 1, 2, 4, and 8 Hz in random order) was investigated in an open-chest dog preparation. CS blood samples were taken before and during the stimulation period for plasma NA and hematocrit determinations. CS blood flow was monitored (extracorporal circulation with an electromagnetic flow meter) and used for NA output computation. The right atrium was paced throughout the experimental period. However, because AV block occurred at a high pacing rate in some amiodarone-treated dogs, pacing rate was lower in that group than in control dogs (132 +/- 13 vs. 161 +/- 10 min-1, ns). Mean arterial pressure was also lower in the treated group (95 +/- 9 vs. 110 +/- 13 mmHg, but increased in every dog upon stimulation (p less than 0.05). Basal left ventricular dP/dtmax was comparable in the two groups of dogs and increased in a similar fashion upon stimulation (p less than 0.05). The increase in plasma NA concentration upon stimulation was comparable between the control and the amiodarone-treated group (0.38 +/- 0.08 vs 0.40 +/- 0.12 ng/mL at 1 Hz and 12.7 +/- 3.1 vs 11.3 +/- 2.3 ng/mL at 8 Hz, ns). The increase in NA output was also comparable (7.0 +/- 1.6 vs. 10.7 +/- 5.4 ng/min at 1 Hz and 356 +/- 124 vs. 334 +/- 102 ng/min at 8 Hz, ns). Amiodarone did not alter the myocardial NA content. We conclude that amiodarone, administered orally for 3 weeks, does not interfere with neural NA release, or with the positive inotropic response, following sympathetic nerve stimulation in dogs.
Amiodarone↗
Corelease of neuropeptide Y like immunoreactivity with catecholamines from the adrenal gland during splanchnic nerve stimulation in anesthetized dogs.
The release of neuropeptide Y like immunoreactivity (NPY-li) from the adrenal gland was studied in relation to the secretion of catecholamines (CA: NE, norepinephrine; E, epinephrine) during the left splanchnic nerve stimulation in thiopental-chloralose anesthetized dogs (n = 16). Plasma concentrations of NE, E, and NPY-li were determined in the left adrenal venous and aortic blood. Adrenal outputs of NPY-li, NE, and E were 2.4 +/- 0.4, 1.4 +/- 0.2, and 7.3 +/- 1.7 ng/min, under basal conditions, respectively. These values increased significantly (p less than 0.05; n = 8) in response to a continuous stepwise stimulation at frequencies of 1, 3, and 10 Hz given at 3-min intervals during 9 min, reaching a maximum output of 4.6 +/- 0.9 (NPY-li), 240.2 +/- 50.2 (NE), and 1412.5 +/- 309.7 ng/min (E) at a frequency of 10 Hz. Burst electrical stimulation at 40 Hz for 1 s at 10-s intervals for a period of 10 min produced similar increases (p less than 0.05) in the release of NPY-li (4.8 +/- 1.0 ng/min, n = 8), NE (283.5 +/- 144.3 ng/min, n = 8), and E (1133.5 +/- 430.6 ng/min, n = 8). Adrenal NPY-li output was significantly correlated with adrenal NE output (r = 0.606; n = 24; p less than 0.05) and adrenal E output (r = 0.640; n = 24; p less than 0.05) in dogs receiving the burst stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)
Adrenal Glands↗
Efficacy of oral sotalol in suppression of premature ventricular complexes and analysis of its beta-adrenergic blocking activity.
The efficacy of oral DL-sotalol in suppressing premature ventricular complexes was assessed by Holter recordings in 28 patients during short term (two weeks) and long term (two years) trials, and its beta-adrenergic blocking effects were evaluated by heart rate response to the Bruce treadmill stress test and plasma catecholamine increases upon active standing. Sotalol produced a significant decrease (more than 85%) in the number of premature ventricular complexes, during both short term (54%) of patients) and long term (39% of patients) trials. The doses employed in this study (320 mg/day) produced mild to moderate degrees of beta-adrenergic blockade as suggested by: a 20% reduction in the mean heart rate on 48 h Holter monitoring (P less than 0.0005); a 15 to 30% reduction in tachycardia induced by strenuous exercise; and a 12% reduction in standing-induced tachycardia. Under long term sotalol therapy the increase in plasma noradrenaline concentrations in response to active standing was not modified, but the increase in plasma adrenaline concentrations was greater than under baseline conditions (P less than 0.025). Both systolic and diastolic blood pressures significantly increased during long term sotalol administration (P less than 0.005 and P less than 0.025, respectively). However, blood pressure remained within the normotensive range during sotalol therapy. It was concluded that sotalol provides, at effective antiarrhythmic doses, a satisfactory level of beta-adrenergic blockade which during standing was associated with significant changes in adrenaline plasma increments.(ABSTRACT TRUNCATED AT 250 WORDS)
Administration, Oral↗
Pre- and postsynaptic adrenergic dysfunctions in hypertension.
Numerous experimental and clinical studies, using various approaches to evaluate the release of sympathetic transmitters and to obtain sympathetic nerve microneurographic recordings, have shown clearly that sympathetic system activity and reactivity is increased in experimental models of hypertension [deoxycorticosterone acetate (DOCA) salt and spontaneously hypertensive rats (SHR)] and in an important subgroup of essential hypertensive patients. This finding may reflect dysfunctions in the baroreflex blood pressure regulation, since an elevated blood pressure should normally inhibit sympathetic activity. This abnormality may arise from a variety of dysfunctions occurring at various sites along the baroreflex arc, including presynaptic modulatory adrenergic autoreceptors, where reduced sensitivity of presynaptic alpha 2 inhibitory receptors and enhanced sensitivity of beta 2 presynaptic receptors have been demonstrated. Although it has been possible to correlate the blood pressure elevation with various indices of sympathetic activity in experimental and human hypertension, the functional implications of that abnormality can be fully understood only in the light of concomitant alterations occurring in postsynaptic mechanisms. Pharmacologic, physiologic and biochemical studies strongly suggest that postsynaptic alpha 1 adrenergic functions become dominant while beta adrenergic functions are attenuated in hypertension. In experimental hypertension, this phenomenon is associated with a reduction in the number of beta adrenoceptors and in the production of its second messenger, cyclic AMP, whereas the number of alpha 1 adrenoceptors remained unchanged or increased, but the production of their second messengers, inositol triphosphate and diacylglycerol, is enhanced in cardiac and vascular tissues. These observations suggest the presence of an imbalance in postsynaptic adrenoceptor functions, which promotes the pressor effects of the sympathetic system.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Predictors of survival and sudden death in patients with stable severe congestive heart failure due to ischemic and nonischemic causes: a prospective long term study of 200 patients.
This prospective study of 200 stable outpatients with New York Hospital Association (NYHA) class III congestive heart failure on maximal medical therapy was done to determine which factors affect survival, to record the incidence of sudden death, and to identify prognostic features which characterize patients at high risk of sudden death. Congestive heart failure was due to coronary artery disease in 151 patients (76%). After an average follow-up of 40 months, 96 patients (48%) had died: 30 (15%) suddenly, 41 (22%) of low output, and 25 (13%) of other causes. Of the 30 patients dying suddenly 12 had autopsies, and acute myocardial infarction was found in nine. Of the 41 patients dying of low output 15 had autopsies, and recent myocardial infarction was found in five. Nine of the 25 patients dying of other causes died of acute myocardial infarction. Multivariate stepwise analysis revealed that severity of ventricular arrhythmias (modified Lown classification), exercise tolerance and left ventricular ejection fraction were the most important determinants of survival. In patients with coronary artery disease, complex ventricular arrhythmias detected by ambulatory Holter monitoring were frequent in all groups and were not clinically useful in predicting which of these patients were at a higher risk of dying suddenly. In contrast, patients without coronary artery disease who died suddenly had a higher incidence of nonsustained ventricular tachycardia and a tendency towards more frequent ventricular arrhythmias in general. The authors conclude that in ambulatory patients with stable NYHA class III heart failure, the severity of ventricular arrhythmias is a predictor of survival.(ABSTRACT TRUNCATED AT 250 WORDS)
Aged↗
The use of angiotensin-converting enzyme inhibitors in congestive heart failure.
The development of angiotensin-converting enzyme (ACE) inhibitors has been important in furthering our understanding of the pathophysiology of congestive heart failure and improving the care of these patients. ACE inhibitors have been shown to improve the longevity and quality of life of patients with congestive heart failure. They decrease neurohumoral over-activation, they restore baroreceptor reactivity, and in many cases they increase sodium and water excretion. If hypovolemia and an excessive decrease in renal perfusion pressure can be avoided, ACE inhibitors generally do not cause a deterioration of renal function and may even improve it. By decreasing myocardial metabolic demand, ACE inhibitors appear to have generally beneficial effects on myocardial metabolic balance. At low perfusion pressures, they also appear to maintain cerebral blood flow.
Angiotensin-Converting Enzyme Inhibitors↗
Blood pressure and plasma catecholamine responses to various challenges during exercise-recovery in man.
The purpose of this study was to assess the effects of a 2 h cycle exercise (50% VO2max) on heart rate (HR) and blood pressure (BP), and on plasma epinephrine (E) and norepinephrine (NE) concentrations, during the recovery period in seven normotensive subjects. Measurements were made at rest in supine (20 min) and standing (10 min) positions, during isometric exercise (hand-grip, 3 min, 25% maximal voluntary, contraction), in response to a mild psychosocial challenge (Stroop conflicting color word task) and during a 5-min period of light exercise (42 +/- 3% VO2max). Data were compared to measurements taken on another occasion under similar experimental conditions, without a previous exercise bout (control). The results showed HR to be slightly elevated in all conditions following the exercise bout. However, diastolic and systolic BP during the recovery period following exercise were not significantly different from the values observed in the control situation. Plasma NE concentrations in supine position and in response to the various physiological and/or psychosocial challenges were similar in the control situation and during the recovery period following exercise. On the other hand plasma E (nmol.1-1) was about 50% lower at rest (0.11 +/- 0.03 vs 0.23 +/- 0.04) as well as in response to hand-grip (0.21 +/- 0.04 vs 0.41 +/- 0.20) and the Stroop-test (0.21 +/- 0.05 vs 0.41 +/- 0.15) following the exercise bout.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Potentiated endothelin-1-induced phosphoinositide hydrolysis in atria and mesenteric artery of DOCA-salt hypertensive rats.
The effect of endothelin-1 on the phosphoinositide pathway was studied in slices of atria and mesenteric artery from normotensive and hypertensive (DOCA-salt) rats. Endothelin-1 induced a dose-dependent increase in inositol monophosphate production in both groups, but the reactivity of the phosphoinositide pathway was enhanced in DOCA-salt hypertensive rats. Endothelin-1 was more potent than noradrenaline and activation by these two agonists combined was additive. The phosphoinositide activation induced by endothelin-1 was independent of extracellular calcium, and was not prevented by nifedipine treatment or by removing calcium from the incubation medium. Endothelin-1 is a potent direct activator of the phosphoinositide pathway in cardiovascular tissues, and this effect is potentiated in DOCA-salt hypertension.
Animals↗
Enhanced sympathoadrenal reactivity to haemorrhagic stress in DOCA-salt hypertensive rats.
The effect of haemorrhagic hypotension on plasma catecholamine levels was studied in anesthetized normotensive and DOCA-salt hypertensive rats. The basal levels of plasma norepinephrine (NE) were significantly higher in DOCA-salt hypertensive rats than in normotensive rats. Moreover, the elevations in plasma NE and epinephrine (E) levels induced by haemorrhagic hypotension were found to be markedly potentiated in DOCA-salt hypertensive rats. Pretreatment with the re-uptake blocker (desmethylimipramine) increased both basal and haemorrhage NE levels in DOCA-salt hypertensive as well as in normotensive rats. Consequently, basal and haemorrhage NE plasma levels remained significantly higher in the DOCA-salt hypertensive animals than in the normotensive rats even following neuronal re-uptake blockage. This suggests that the elevated NE concentrations found in the plasma of DOCA-salt hypertensive rats both under basal condition and during haemorrhagic hypotension do not reflect a defective re-uptake. Moreover, in contrast with what is observed in normotensive animals, bilateral adrenalectomy did not induce any increase in basal or haemorrhage NE levels in the DOCA-salt hypertensive rats. This constitutes yet more evidence supporting the existence of an impaired balance of the sympatho-adrenal axis in this hypertension model. The present study therefore suggests that the potentiated plasma catecholamine response to haemorrhage in DOCA-salt hypertensive rats is the consequence of an increased sympathoadrenal reactivity and not of an altered neuronal uptake. This hyperreactivity may result from an impaired regulation of the sympatho-adrenal axis in that hypertension model.
Adrenal Medulla↗
Peripheral neurogenic mechanisms in deoxycorticosterone acetate--salt hypertension in the rat.
The finding of elevated circulating catecholamine levels in experimental and human hypertension suggests an active sympathoadrenal participation in the pathogenesis of hypertension. In deoxycorticosterone acetate (DOCA)-salt hypertensive rats and in spontaneously hypertensive rats (SHR) the sympathoadrenal reactivity was found to be potentiated in response to various stimuli suggesting alterations in baroreflex functions or in local modulatory mechanisms. Several studies have suggested an attenuation of the alpha 2-presynaptic or local inhibitory mechanism and a potentiation of the beta 2-facilitatory presynaptic mechanism in the peripheral sympathetic system, thus possibly explaining the potentiated sympathoadrenal reactivity in those hypertensive animals. At postsynaptic adrenergic sites, beta-adrenoceptor numbers were reported to be decreased, whereas alpha 1-adrenoceptor numbers were unchanged in the cardiovascular system of DOCA hypertensive rats, thus favoring a dominance of alpha 1-postsynaptic responses in those animals. In support of this concept, the production of inositol monophosphate, used as an index of inositol triphosphate production, was found to be markedly enhanced following norepinephrine-induced alpha 1-stimulation in atria and ventricles as well as in mesenteric and femoral arteries of DOCA-salt hypertensive rats thus suggesting an increased reactivity of the second messenger system linked to alpha 1-adrenoceptors. Since similar abnormalities were also observed in SHR and in human hypertension, it thus appears that an imbalance between alpha- and beta-postsynaptic receptors may exist in various forms of hypertension. These studies therefore suggest the existence of multiple abnormalities in pre- and post-synaptic adrenergic mechanisms in experimental and human hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
Desoxycorticosterone↗
The sympatho-adrenal tone and reactivity in human hypertension.
In the last two decades, remarkable advances have permitted a better understanding of the modulation of sympathetic tone and reactivity at the sympathetic nerve and at the effector cell levels. In man, several indirect approaches have permitted to suggest the possibility of increased sympathetic nerve activity and reactivity in an important subgroup of essential hypertensive patients. The demonstration of significant correlations between circulating levels of sympathetic transmitters and various parameters of cardiovascular functions supports the hypothesis of a participation of the sympathetic system in the maintenance of an elevated blood pressure in those patients. Moreover, several experimental evidences have indicated that the sensitivity of cardiovascular effector cells may be altered in hypertensive patients. The blunted beta receptor responsiveness and the normal or enhanced alpha receptor responsiveness which were observed suggest the possibility of an imbalance between adrenergic receptor functions in hypertension, which may explain the preferential alpha 1 modulation of blood pressure through changes in peripheral resistance in hypertensive patients. Such an abnormality could contribute to the development of cardiac and vascular wall hypertrophy during the evolution of hypertension. These studies therefore suggest that a variety of sympathetic dysfunctions could play a role in the development, maintenance and evolution of human essential hypertension.
Adrenal Glands↗