Vascular reactivity in essential and renal hypertension in man

Mendlowitz, Milton

doi:10.1016/0002-8703(67)90317-1

Cited by 24 publications

(3 citation statements)

References 67 publications

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“…The vascular reactivity to catecholamines has been found to increase in DOCA and sodium hypertension (15)(16)(17) as well as in by guest on May 11, 2018 http://circres.ahajournals.org/ Downloaded from other forms of hypertension (15)(16)(17)(18)(19)(20), and to decrease during sodium deprivation (21,22) and after treatment by natriuretic agents (20,23,24). It is not known to what extent the subcellular distribution of norepinephrine may be related to the state of vascular reactivity, but in these conditions it seems that the change in responsiveness could be associated with changes in subcellular distribution of the catecholamine.…”

Section: Discussionmentioning

confidence: 99%

Relationship between Sodium Intake and Norepinephrine Storage during the Development of Experimental Hypertension

Champlain

Krakoff

Axelrod

1968

Circulation Research

130

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It has been reported that storage of norepinephrine by the sympathetic nervous system was decreased in rats made hypertensive by the administration of desoxycorticosterone trimethylacetate (DOCA) and sodium chloride. The present investigation indicated that the storage of norepinephrine was impaired at an early stage of treatment with DOCA and NaCl (1 week), and preceded the appearance of hypertension. The role of sodium and sympathetic activity, the two major factors suspected of contributing to the development of the abnormality in storage of norepinephrine, was studied in normotensive and hypertensive rats. The withdrawal of sodium from the diet of hypertensive rats for 2 weeks lowered the blood pressure to normotensive levels and simultaneously restored to normal the storage and binding capacity as well as the endogenous norepinephrine content of the sympathetic storage granules in the heart. Sodium restriction or depletion in normotensive rats caused a slight decrease in blood pressure and the retention of norepinephrine in the storage granules was increased. These findings suggested that the capacity of the sympathetic granules to bind and store norepinephrine was influenced by the state of sodium balance and showed that the capacity of storage could be correlated with the level of blood pressure. The finding that treatment with a long-acting ganglionic blocker could restore the blood pressure and the norepinephrine storage capacity in hypertensive animals to normal suggested a neurogenic component in the development of this form of hypertension. obtain further information concerning the sequence of events occurring during the development of this form of hypertension and the role of sodium intake in the production of this abnormality in norepinephrine storage. The production of hypertension in animals treated with DOCA and NaCl is associated with sodium retention. Furthermore, the sodium and potassium contents of vascular tissues are increased in this form of hypertension as well as in other forms of hypertension in humans and experimental animals (4-8). It is therefore possible that a disturbance in the intraneural ionic balance is responsible for the decreased capacity of the adrenergic nerve to store norepineph- ADDITIONAL KEY WORDS

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Section: Discussionmentioning

confidence: 99%

Relationship between Sodium Intake and Norepinephrine Storage during the Development of Experimental Hypertension

Champlain

Krakoff

Axelrod

1968

Circulation Research

130

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“…18 All investigators appear to agree that the emotional responses are maladaptive although there has been no unanimity as to the specific nature of the response.'" 6 Another methodologic problem may have contributed to the confusion. An important element of selection is built into the referral process, 4 as is most clearly seen in the early literature on hypertension; patients selected for referral to a psychiatrist are not a random sample.…”

Section: Figure 3 Influence Of Control Plasma Renin Activity and Plamentioning

confidence: 99%

Essential hypertension: abnormal renal vascular and endocrine responses to a mild psychological stimulus.

Hollenberg¹,

Williams²,

Adams³

1981

Hypertension

158

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SUMMARYWe have assessed the influence of a mild emotional stimulus on arterial blood pressure, heart rate, renal blood flow, plasma resin activity (PRA), and plasma aldosterone concentration in 24 normal subjects, eight of whom had a parent with hypertension, and in IS patients with essential hypertension. A nonverbal IQ test, Raven's Progressive Matrices, was employed as the stimulus. In 11 of the 15 hypertensives, arterial blood pressure rose transiently by 7 mm Hg or more, but in only three of 16 normal subjects (x 2 = 7.23, p < 0.01). Transient moderate increases in heart rate were also more common in the hypertensives (p < 0.01). Renal blood flow rose in 11 of 16 normal subjects and fell in each of the 15 patients with essential hypertension (x* -15.1;/> < 0.005). As opposed to the transient changes in arterial pressure and heart rate, the fall in renal perfusion was sustained. The PRA fell in 10 of the 16 normal subjects with a negative family history and rose In 14 of 15 patients with essential hypertension (p < 0.005). Changes in plasma angiotensin II concentration and in plasma aldosterone were in accord with the changes in PRA, but plasma cortisol did not change. Both the renal vascular response and the change in PRA were intermediate in normal subjects in whom family history was positive for hypertension. For the entire group of 39 subjects there was statistically significant agreement between the direction of the renal vascular response and the directional change in PRA: renal blood flow rose when PRA fell and fell when PRA rose (p < 0.005). We conclude that there is an abnormality in the control of both the renal circulation and of renin release in patients with essential hypertension in response to psychological provocation, and that a similar process is present in some normotensive subjects whose parents have hypertension. (Hypertension 3: 11-17, 1981) KEY WORDS • emotions• familial hypertension renal vasculature • plasma renin activity • plasma aldosterone E SSENTIAL hypertension remains a disease of unknown pathogenesis. As for many processes in which the cause is obscure and which may be exacerbated by stressful circumstances, investigators have repeatedly claimed that psychological, especially emotional, factors play a pathogenetic role -perhaps the key role.1 "' As reviewed recently,*"' this conclusion has lacked credibility to many for a number of reasons: the conclusions were often based on subjective and uncontrolled observations and the stimuli employed were often gross and poorly reproducible. Moreover, the inFrom the

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“…This marked increase in PNA levels in response to exercise after long-term treatment with beta blocking agents has been found too by Klein et al (1976) and Hansson and H6kfelt (1975) and H6kfelt et al (1975). In addition, an increased vascular reactivity to PNA (Doyle et al, 1959 ;Mendlowitz, 1967) may also play a role within this regulating mechanism. After long-term treatment SN activity is decreased under basal conditions; the regulatory reflex mechanism seems to be untouched by beta blocking agents.…”

Section: Mean Arterial Bp I Mmhg)mentioning

confidence: 99%

Decrease in plasma noradrenaline levels following long-term treatment with prindolol in patients with essential hypertension

1976

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15 patients (4 females, 11 males, 21 to 55-year old) with mild to moderate essential hypertension (EH) were treated with placebo for two weeks and thereafter with increasing doses of prindolol (15 to 38 mg/day in the mean) and kept on a mean maintenance dosage of 32 mg/day for an average of 16 weeks in all. Blood pressure (BP), heart rate und plasma noradrenaline (PNA) concentrations were measured under standardized conditions (supine, standing, walking) at the end of two weeks on placebo and after the experimental treatment period. The results were compared to those of a group of 15 normotensive untreated control subjects (NS): after an average of 16 weeks on prindolol BP fell from 163/113 mm Hg to 129/91 mm Hg in the mean. PNA levels in EH before prindolol were significantly higher than in NS (supine: 272 +/- 22.0 ng/l (mean +/- SEM) vs. 135 +/- 15.1 ng/l, standing: 448 +/- 31.9 ng/l vs. 359 +/- 18.4 ng/l, walking: 388 +/- 22.5 ng/l vs. 234 +/- 22.1 ng/l). In EH chronic administration of prindolol led to a significant decrease in PNA concentrations under all the three test conditions to levels which did not differ significantly any more from those derived from NS. The adrenergic response to upright posture reflected in the percentage increase in PNA was significantly less in EH before prindolol when compared to the percentage increase in NS. On prindolol the adrenergic response was not abolidhed, yet it tended to approach the values found in NS. Before prindolol under resting conditions diastolic BP correlated closely with the corresponding PNA levels (p less than 0.01, r = 0.66, n = 15). This correlation could not be reestablished after prindolol treatment. The decrease in PNA after long-term treatment with prindolol was not correlated to the fall in blood pressure. The decrease in PNA indicates a lower activity of the sympathetic nervous system which may contribute to the antihypertensive effect of prindolol.

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Vascular reactivity in essential and renal hypertension in man

Cited by 24 publications

References 67 publications

Relationship between Sodium Intake and Norepinephrine Storage during the Development of Experimental Hypertension

Relationship between Sodium Intake and Norepinephrine Storage during the Development of Experimental Hypertension

Essential hypertension: abnormal renal vascular and endocrine responses to a mild psychological stimulus.

Decrease in plasma noradrenaline levels following long-term treatment with prindolol in patients with essential hypertension

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