Autonomic and Non-Autonomic Circulatory Components in Essential Hypertension in Man

Pi, Korner; Shaw, John H.; Uther, John B.; West, MJ; McRitchie, R. J.; Richards, John

doi:10.1161/01.cir.48.1.107

Cited by 103 publications

(35 citation statements)

References 21 publications

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“…In early hypertension, there are signs of a net increase of adrenergic influence on the heart (Julius et al, 1971) but, at least in established hypertension, this seems to be due more to a withdrawal of parasympathetic rather than to an increase of sympathetic tone (Korner et al, 1973). The increased sympathetic activity in brain arteries of adult SHR (Sadoshima and Heistad, 1982;Mueller and Ertel, 1983) is, however, accompanied by an increase of sympathetic vasoconstrictor nerves in most, and a greater decrease of nonsympathetic vasodilator nerves in some, brain regions.…”

Section: Resultsmentioning

confidence: 99%

Altered cerebral vessel innervation in the spontaneously hypertensive rat.

Lee¹,

Saito²

1984

Circulation Research

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SUMMARY. Autonomic innervation in the cerebral arterial walls of adult male spontaneously hypertensive rats and of normotensive Wistar-Kyoto rats was studied. When examined by fluorescence microscopy, dense catecholamine fluorescence was observed in anterior cerebral and middle cerebral arteries of both Wistar-Kyoto and spontaneously hypertensive rats. However, vertebral and basilar arteries and small pial arteries of Wistar-Kyoto rats received extremely sparse or no catecholamine fluorescence, whereas, in the respective regions of spontaneously hypertensive rats, catecholamine fluorescence was found to be significantly elevated. The endogenous norepinephrine content was also higher in cerebral arteries of spontaneously hypertensive than of Wistar-Kyoto rats. When examined ultrastructurally (potassium permanganate fixation), the incidence of granular vesicle-containing nerves, indicative of sympathetic nerves, was found to be significantly elevated in all cerebral arteries of spontaneously hypertensive rats examined. In contrast, the agranular vesicle-containing nerve, indicative of nonsympathetic nerves, with close synaptic cleft distance (<2 /im) was found to decrease or remain unchanged in the cerebral arteries of spontaneously hypertensive rats. These results suggest that cerebral sympathetic vasoconstriction may become more prominent than nonsympathetic vasodilation in spontaneously hypertensive rats. This finding lends further credence to the previous in vivo findings that cerebral sympathetic vasoconstrictor nerves become more functional and exhibit a protective effect against brain lesions during hypertension. The potential roles of neurogenic components involved in cerebral blood flow autoregulation are also discussed. (Circ Res 55: 392-403, 1984)

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Section: Resultsmentioning

confidence: 99%

Altered cerebral vessel innervation in the spontaneously hypertensive rat.

Lee¹,

Saito²

1984

Circulation Research

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“…On the second day after another set of control observations the subject was given atropine (0.04 mg/kg i.v. in a dose to block reflex vagal effects on heart rate, Korner et al, 1973Korner et al, , 1976 followed by another set of resting and exercise measurements; the protocol was repeated 30 min after injecting 5 mg i.v. pindolol.…”

Section: Exercise Studies With Atropinementioning

confidence: 99%

Pindolol pharmacokinetics in relation to time course of inhibition of exercise tachycardia.

Jennings¹,

Bobik²,

Fagan³

et al. 1979

Brit J Clinical Pharma

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1 Pharmacokinetics of pindolol were studied in normal subjects given 5, 10 and 20 mg orally and 3 mg i.v. Plasma half time was 2.9 +/‐ 0.3 (s.e. mean) h for both routes; peak drug levels occurred 1–2 h after ingestion and bioavailability was 53%. Plasma protein binding was 38% and was independent of plasma concentration; the drug was not concentrated in the red cell. 2 Work‐heart rate regression lines were calculated from resting heart rate and three grades of 'steady‐state' exercise standardized for the maximum work capacity (Wmax) of each subject. The equation was characterized by slope and HR50 (calculated heart rate at 0.5 Wmax). 3 After giving 5 mg i.v. pindolol to produce maximum cardiac beta‐adrenoceptor blockade there were differences in inhibition of resting heart rate, slope, HR50 and maximum heart rate suggesting differences in sympathetic components. However, estimates of the degree of inhibition were closely similar for each variable when determined before and after atropinization indicating that the accuracy of estimation was independent of the level of vagal activity. 4 After oral pindolol peak inhibition of resting heart rate, slope and HR50 coincided with peak plasma concentration. Peak reduction of resting heart rate was greatest at the lowest dose, but inhibition of slope and HR50 were similar at all doses. 5 The different heart rate parameters recovered at different rates. After 24 h slope had returned to control, and the residual inhibition of HR50 reflected residual beta‐ adrenoceptor blockade of resting heart rate, as demonstrated by a shift in isoprenaline‐heart rate relationship. 6 Inhibition of HR50 and other exercise parameters were 20% less in the concentration range 5–20 ng/ml than peak inhibition obtained in the range 21–160 ng/ml. The higher potency of pindolol compared with propranolol can be accounted for by the difference in protein binding.

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“…The increased heart rate in borderline hypertensive subjects (Frohlich, Kozul, Tarazi & Dustan, 1970;Berglund, Wilhelmsen & Werko, 1974) and in established hypertension (Isacsson, 1972) has been taken as indirect evidence of increased sympathetic activity, as has also the increased cardiac output in hypertensive patients without organ damage (Sannerstedt, 1969). Haemodynamic studies, however, have shown the hyperkinetic circulation in labile as well as in established hypertension to be caused by a combination of increased sympathetic activity and decreased parasympathetic tone (Julius, Pascual & London, 1971 ;Korner, Shaw, Uther, West, McRitchie & Richards, 1973). Direct quantification of sympathetic nervous system activity by insertion of needle electrodes into efferent sympathetic nerves has not shown any increase (G. Wallin, W. Delius & K. E. Hagbarth, unpublished work).…”

Section: Introductionmentioning

confidence: 99%

Urinary Noradrenaline Excretion and Renal Function in Normal and Hypertensive 50-year-Old Men

1975

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1. Sympathetic nervous system activity, measured by urinary noradrenaline excretion, was determined in a group of untreated hypertensive subjects (n = 35), a reference group (n = 80) and a normotensive group (n = 51), all derived from a random population sample of 50-year-old men. It was compared with casual and resting blood pressure, urinary sodium excretion, urinary cretinine concentration and glomerular filtration rate. Hypertension was defined as systolic pressure greater than 175 or diastolic greater than 115 mmHg on two separate occasions. Normotension was defined as systolic pressure less than 160 and diastolic pressure less than 95 mmHg. 2. There was no difference in the average excretion of noradrenaline during the day or night between the reference, normotensive and hypertensive groups. None of the hypertensive patients had values for urinary noradrenaline excretion during the day above the range found in normotensive subjects, indicating that hypertension with increased sympathetic nervous system activity is uncommon when hypertension in defined as above. 3. No correlation between urinary noradrenaline excretion during the day and blood pressure was found in the reference group or in the normotensive group. In the hypertensive group, there was a negative correlation between urinary noradrenaline excretion and blood pressure after rest. This finding might indicate that factors other than sympathetic nervous system activity determine the level of blood pressure in hypertensive subjects. 4. In the hypertensive group, urinary noradrenaline excretion during the day was positively correlated with both urinary sidium excretion during the day and glomerular filtration rate. Urinary noradrenaline excretion per 24 h was positively correlated with urinary sodium excretion during the same time. High resting blood pressure, low urinary sodium excretion, low glomerular filtration rate and a reversed diurnal rhythm of urinary excretion characterized hypertensive patients with low urinary noradrenaline excretion, indicating more severe hypertension in these hypertensive patients with reduced sympathetic nervous system activity.

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Autonomic and Non-Autonomic Circulatory Components in Essential Hypertension in Man

Cited by 103 publications

References 21 publications

Altered cerebral vessel innervation in the spontaneously hypertensive rat.

Altered cerebral vessel innervation in the spontaneously hypertensive rat.

Pindolol pharmacokinetics in relation to time course of inhibition of exercise tachycardia.

Urinary Noradrenaline Excretion and Renal Function in Normal and Hypertensive 50-year-Old Men

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