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PubMedDate not supplied

Carvedilol improves left ventricular function in heart failure patients with idiopathic dilated cardiomyopathy and a wide range of sympathetic nervous system function as measured by iodine 123 metaiodobenzylguanidine.

BACKGROUND: Carvedilol treatment reduces the mortality rate in patients with congestive heart failure. It is not known whether carvedilol treatment is effective in heart failure patients with substantial cardiac sympathetic nerve dysfunction. The goal of this study was to determine the effect of chronic carvedilol treatment in patients with cardiac sympathetic nerve dysfunction of varying severity. METHODS AND RESULTS: In 22 congestive heart failure patients with idiopathic cardiomyopathy, sympathetic nerve function was assessed before and after 7.2 +/- 2.7 months of carvedilol treatment with the use of iodine 123 metaiodobenzylguanidine (MIBG) imaging, radionuclide ventriculography, and transmyocardial norepinephrine sampling. Patients with relatively advanced impairment of cardiac sympathetic nerve function, as manifested by a baseline I-123 MIBG ratio lower than 1.40, had a statistically significant improvement in I-123 heart-mediastinum ratio with carvedilol treatment, from 1.26 +/- 0.12 to 1.39 +/- 0.20 (P =.004). Of 10 patients with a baseline I-123 MIBG ratio lower than 1.40, 9 had an increase in the heart-mediastinum ratio with carvedilol treatment. Left ventricular ejection fraction increased from 25.4% +/- 7.8% to 37.3% +/- 14.7% (P <.001), with no difference between patients with relatively advanced versus relatively preserved cardiac sympathetic nerve function. CONCLUSION: Most patients with congestive heart failure show a favorable response in left ventricular function to carvedilol treatment, regardless of the baseline level of cardiac sympathetic nervous system function, as assessed by neuronal imaging with I-123 MIBG. Patients with relatively advanced impairment of baseline I-123 MIBG uptake are most likely to show evidence of improved cardiac sympathetic nervous system function in response to carvedilol therapy.

3-Iodobenzylguanidine↗
PubMed1990

Decreased angiotensin II receptors in subfornical organ of spontaneously hypertensive rats after chronic antihypertensive treatment with enalapril.

Angiotensin II (ANG II) receptor density was higher in many brain regions of untreated spontaneously hypertensive rats (SHR) compared to untreated Wistar-Kyoto (WKY) animals. Systemic inhibition of angiotensin converting enzyme with enalapril (25 mg/kg, per os for 14 days) produces a large decrease in ANG II receptors localized exclusively in the subfornical organ (SFO) of the SHR, and no alterations in ANG II receptors in the normotensive WKY rats. Selective decrease of ANG II receptors in the SFO of the genetically hypertensive rats with enalapril may be related to its therapeutic efficacy.

Angiotensin II↗
PubMed1993

Features of systemic sclerosis (scleroderma) in an identical twin pair.

The aetiology of systemic sclerosis (scleroderma) is unknown but it is thought to have both genetic and environmental components. The familial incidence of the disease is very low and we have been able to find only one report of scleroderma in identical twins which was in the Russian literature. We report here on a set of identical twins and their mother who all had features of systemic sclerosis.

Adolescent↗
PubMed2002

The influence of central command on baroreflex resetting during exercise.

The arterial baroreflex functions as a negative feedback system regulating blood pressure around an established operating point. Paradoxically, a parallel increase in heart rate and blood pressure manifests during exercise. Experimental evidence suggests these events are caused, in part, by a rapid resetting of the baroreflex by central command.

Animals↗
PubMed1999

Effects of sodium depletion on the role of AT1- and alpha-adrenergic receptors in the regulation of forearm vascular tone in humans.

OBJECTIVE: Sodium depletion stimulates the renin-angiotensin and sympathetic nervous systems, which may affect the role of each of these systems in the regulation of vascular tone. We investigated the influence of sodium depletion on the roles of the angiotensin II type 1 receptor and the alpha1- and alpha2-adrenergic receptors, and on nitric oxide generation, in the regulation of human forearm vascular tone. SUBJECTS AND METHODS: We studied the effects of the angiotensin II type 1 receptor antagonist losartan (0.1-3 microg/kg per min), angiotensin II (0.01-10 ng/kg per min), the alpha1- and alpha2-adrenoceptor antagonists doxazosin (3-100 ng/kg per min) and yohimbine (0.5-4 microg/kg per min) and the nitric oxide synthase inhibitor N(G)-monomethyl-L-arginine (L-NMMA; 7.5-60 microg/kg per min) on forearm blood flow in control subjects (n = 12) and sodium-depleted subjects (n = 11). Sodium depletion was achieved by 3 days of pretreatment with 40 mg furosemide twice a day and a sodium-restricted diet. Forearm blood flow was measured by venous occlusion plethysmography. RESULTS: Sodium depletion resulted in activation of the renin-angiotensin and sympathetic nervous systems, as indicated by increased levels of plasma renin, aldosterone and heart rate (P < 0.05). Blood pressure remained unchanged. Losartan at the highest dose increased forearm blood flow in the sodium-depleted group by 42 +/- 9%, but had no effect in controls (P < 0.05). Both doxazosin and yohimbine caused an increased vasodilatory effect in the sodium-depleted versus the control group (228 +/- 42 versus 83 +/- 13% and 192 +/- 24 versus 95 +/- 8%, respectively; P < 0.05). The constrictor effects by angiotensin II and L-NMMA of -65 +/- 6% and -79 +/- 4%, respectively, in controls were unchanged by sodium depletion. CONCLUSIONS: In sodium-depleted subjects, endogenous angiotensin II appears to play a role in the regulation of forearm vascular tone, in contrast to sodium-replete conditions. Furthermore, in these subjects the role of alpha1- and alpha2-adrenoceptors in the regulation of forearm vascular tone was enhanced compared with control conditions. Neither the forearm vascular effects of exogenously infused angiotensin II nor those of baseline nitric oxide production were influenced by sodium depletion.

Adrenergic alpha-Antagonists↗