Effect of Prolonged Treatment on Hæmodynamics of Essential Hypertension Before and After Autonomic Block

Jennings, G. L.; Esler, M.; Pi, Korner

doi:10.1016/s0140-6736(80)90059-8

Cited by 32 publications

(6 citation statements)

References 19 publications

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“…1 " 4 The findings suggested that the longer the period of treatment, the greater the degree of regression of cardiovascular hypertrophy. 4 - 5 Normally, in chronic hypertension, hypertrophy is associated with the well-known structural changes of the resistance vessels, with narrowing of the lumen and an increase in wall/lumen ratio.…”

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confidence: 98%

Enalapril can prevent vascular amplifier development in spontaneously hypertensive rats.

1990

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Three groups of spontaneously hypertensive rats (SHR) were given enalapril (25 mg/kg/day) from 4 to 9 weeks, 4 to 14 weeks, and 14 to 20 weeks of age. The drug was stopped and observations continued for another 16-21 weeks. At selected times, we measured blood pressure, in vitro hindquarter vascular resistance properties, left ventricular weight/body weight ratio, and skeletal muscle vessel norepinephrine kinetics in treated and untreated SHR and in Wistar-Kyoto (WKY) rats. At the end of each treatment period, all cardiovascular variables were close to values of WKY rats and well below those of untreated SHR, and the norepinephrine or fractional rate constant was about 25% below those levels. After enalapril was stopped, blood pressure and left ventricular weight/body weight ratio increased in parallel to levels ranging from 30% to 50% of the normal difference between untreated SHR and WKY rats. However, in SHR treated from 4 to 9 weeks and from 4 to 14 weeks of age, hindquarter resistance properties remained close to WKY rat levels for the entire observation period of 16-21 weeks after treatment, suggesting suppression of the enhanced resistance responses of SHR (amplifier properties). In SHR treated from 14 to 20 weeks of age, suppression of amplifier properties was more transient, and they redeveloped partially 5-6 weeks after cessation of therapy. When enalapril was given up to 14 weeks of age, the long-term suppression of amplifier properties was probably mainly through prevention of smooth muscle hypertrophy in resistance vessels and possibly through other mechanisms (eg., "rarefaction"). After that age, its therapeutic action was similar to that of other antihypertenslve drugs where, after drug withdrawal, there is a slow pressure rise in parallel with redevelopment of vascular and cardiac hypertrophy. (Hypertension 1990;16:252-260)

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confidence: 98%

Enalapril can prevent vascular amplifier development in spontaneously hypertensive rats.

1990

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“…In another group of 13 patients blood pressure was well controlled over a period of 1 year (Jennings et a/. 1980).…”

Section: L Omentioning

confidence: 96%

Role of Cardiac and Vascular Amplifiers in the Maintenance of Hypertension and the Effect of Reversal of Cardiovascular Hypertrophy

Jennings

Esler

et al. 1985

Clin Exp Pharma Physio

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Changes in amplifying capacities of the hypertrophied heart and resistance vessels account for the characteristic evolution of haemodynamic patterns in the course of essential hypertension. Reversal of hypertrophy in established essential hypertension requires prolonged control of blood pressure. Redevelopment of hypertension on stopping drug therapy is slowest if there has been reversal of both vascular and cardiac hypertrophy. It may be possible to subsequently maintain normal blood pressure in a proportion of patients by non-pharmacological means following the initial period of drug therapy. Preliminary findings suggest that in a majority of patients the sympathetic nervous system may be overactive, whilst a smaller subset may have dysfunction of volume regulation.

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“…Renal denervation can improve vascular peripheral stiffness with a reduction of pulse wave velocity. 65,66 Therefore, reversal of peripheral vascular remodeling as observed also after effective BP reduction with drugs 67 could be involved in the late improvement in BP. Also other underestimated factors, such as vitamin D deficiency 68 and other unrecognized confounders, may also limit the BP response to renal denervation.…”

Section: Variability Of Bp Responsesmentioning

confidence: 99%

Renal Denervation for the Treatment of Cardiovascular High Risk-Hypertension or Beyond?

Böhm

Linz

Ukena

et al. 2014

Circulation Research

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Hypertension imposes a major burden of morbidity and mortality and is associated with sympathetic nervous system overactivity. Renal sympathetic denervation has been shown to reduce office blood pressure, ambulatory blood pressure, and sympathetic activity in patients with resistant hypertension. Therefore, the procedure has attracted a lot of attention. Beyond blood pressure, renal denervation has been shown to improve glucose tolerance, microalbuminuria, and arrhythmias in several experimental models and, in admittedly, often uncontrolled clinical studies. It has been demonstrated to reduce myocardial hypertrophy in a blood pressure–independent and blood pressure–dependent way. The first studies on heart failure with preserved and reduced ejection fraction are ongoing. Renal sympathetic denervation holds promise for future indications in hypertension and related comorbidities and consequences, such as metabolic disease, renal failure, and heart failure. Published data in a placebo-control blinded study, however, are needed. The aim of this review is to provide a critical and comprehensive overview of heretofore generated data on renal denervation in experimental models, in human hypertension, and on early developments in new indications, which should indicate the way to powered and performed, controlled clinical studies appropriately.

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Effect of Prolonged Treatment on Hæmodynamics of Essential Hypertension Before and After Autonomic Block

Cited by 32 publications

References 19 publications

Enalapril can prevent vascular amplifier development in spontaneously hypertensive rats.

Enalapril can prevent vascular amplifier development in spontaneously hypertensive rats.

Role of Cardiac and Vascular Amplifiers in the Maintenance of Hypertension and the Effect of Reversal of Cardiovascular Hypertrophy

Renal Denervation for the Treatment of Cardiovascular High Risk-Hypertension or Beyond?

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