摘要:

Sexual dysfunction is common in hypertensive men and often is first reported by patients while receiving hypotensive therapy, leading to a widespread belief by patients and physicians that the sexual dysfunction is caused by a specific antihypertensive medication. However, it is unclear from the literature whether this problem is related to hypertension or to its therapy. Further, whether the erectile failures reported during therapy are a result of 1) reduced penile blood flow secondary to reduction of blood pressure after antihypertensive treatment or to obstructive vascular disease (or both) or 2) specific drug effects has not been well studied. Because of these unresolved issues, this common problem is not well managed and contributes to noncompliance with therapy by hypertensive male patients, which impedes the attainment of satisfactory Mood pressure control. The present article reviews the literature related to hypertension and sexual function in men and outlines a management strategy for clinicians that attempts to document normalcy of sexual function before initiating treatment in newly diagnosed hypertensive patients. Further, it does not ascribe causality to specific antihypertensive agents for the sexual dysfunction reported by treated hypertensive patients but attempts instead to delineate the pathogenesis of the dysfunction. Once the pathogenesis is established, treatment plans can be implemented to restore normotension and maintain adequate sexual function among treated hypertensive men. The article also discusses how applied research in this area may be performed.

ISSN:0194-911X    

出版商:OVID    

年代:1988

数据来源: OVID

ISSN:0194-911X    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

The circadian blood pressure rhythm was compared in patients with Cushing's syndrome, essential hypertension, and primary aldosteronism. In patients with essential hypertension or primary aldosteronism, a dear nocturnal fall in systolic and diastolk blood pressure and heart rate was observed. This fall was seen in untreated subjects as well as in patients receiving combined treatment with a calcium antagonist, diuretic, converting enzyme inhibitor, α-locker and β-blocker, or sympatholytic drug. In these groups, there was a positive correlation between heart rate and systolic or diastolic blood pressure. On the other hand, in patients with Cushing's syndrome, there was no nocturnal fall in blood pressure but in some patients a rise was observed. In all patients there was a nocturnal fall in heart rate. Thus, there was no significant correlation between heart rate and blood pressure in these patients. Exogenous glucocortkoid eliminated the normal nocturnal fall of blood pressure in patients with chronic glomerulonephritis or systemic lupus erythematosus. These results suggest that the changed circadian blood pressure pattern in patients with Cushing's syndrome is not due to antihypertensive treatment or to the mineralocorticold excess accompanying this disease, but it is attributable to excess glucocorticoid or the associated disturbance in the adrenocorticotropic hormone-glucocorticoid system (or both). This conclusion also implies that the normal circadian rhythm of blood pressure may be regulated at least in part by the adrenocorticotropic hormone-glucocorticoid system.

ISSN:0194-911X    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

To assess the effects of vasopressors on plasma levels of immunoreactive atrial natriuretk factor (ANF), 13 normal men were studied on two occasions. On the experimental day, subjects received sequential 15-minute intravenous infusions of angiotensin II in doses of 4, 8, and 16 pmol/kg/min. Following a 30-minute recovery period, subjects received sequential 15-minute infusions of phenylephrine in doses of 0.4 and 0.8 μg/kg/min. Right atrial pressure, mean pulmonary capillary wedge pressure, pulmonary artery pressure, mean systemic arterial pressure, and plasma levels of renin activity, aldosterone, angiotensin II, and immunoreactive ANF were obtained sequentially throughout the protocol. During the control day, vehicle was infused and plasma samples were obtained for hormone measurements. Infusion of angiotensin II and phenylephrine increased mean systemic arterial pressure in a stepwise fashion. Both right atrial pressure and pulmonary capillary wedge pressure increased significantly during both doses of phenylephrine, but only the highest dose of angiotensin II significantly increased atrial pressures. Plasma levels of immunoreactive ANF increased in parallel with the changes in right atrial pressure and pulmonary capillary wedge pressure, with significant increases occurring only at the highest dose of both pressors. Angiotensin II and aldosterone levels increased and renin activity decreased during infusion of angiotensin II. There were no significant changes in plasma levels of immunoreactive ANF during the control day. These studies demonstrate that infusion of vasopressors increases plasma levels of ANF, but only when the vasopressor effect is associated with significant increases in right atrial and pulmonary capillary wedge pressures. Atrial stretch is the most likely mediator of the Increase in plasma levels of immunoreactive ANF during vasoconstriction.

ISSN:0194-911X    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

Intraceilular sodium, potassium, and free calcium concentrations were investigated in lymphocytes of 30 patients with essential hypertension and 30 normotensive controls. All subjects were placed on a diet containing 8 to 10 g of sodium chloride per day. Lymphocyte sodium concentration was higher in hypertensive patients than in normotensive controls (19.8 ± 1.8 vs 18.4 ± 1.8 mmol/kg wet weight;p< 0.01), whereas lymphocyte potassium concentration was similar in both groups. Lymphocyte free calcium concentration was also higher in hypertensive patients than in normotensive controls (134.6 ± 13.2 vs 120.2 ± 16.4 nmol/L;p< 0.01). There was a positive correlation between lymphocyte sodium and free calcium concentrations in normotensive controls, in hypertensive patients, and in the subjects combined (r = 0.59,p< 0.01;r= 0.71,p< 0.001; andr= 0.70,p< 0.001, respectively). Lymphocyte potassium concentration was not related to lymphocyte sodium or free calcium concentration in each group. In patients with essential hypertension, intraceilular sodium and free calcium concentrations were negatively correlated with plasma renin activity (r= −0.66,p< 0.001;r= −0.60,p< 0.001, respectively), but they were not related to age, mean blood pressure, serum electrolyte concentration, or plasma norepinephrine concentration. These results suggest that a considerable relationship exists between intraceilular sodium and free calcium in lymphocytes and that, in essential hypertension, the alteration in cellular metabolism of sodium and calcium may be linked to the renin system but not to blood pressure, age, or adrenergic activity.

ISSN:0194-911X    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

We investigated the effects of plasma from dogs with perinephritk hypertension on the Na+-K+pump of cultured dog vascular smooth muscle cells. We also measured [3H]ouabaln binding by myocardium and vascular tissue. Fresh, unprocessed plasma from healthy dogs during the first 6 weeks of benign one-kidney, one wrapped hypertension and from paired normotensive control dogs was layered over confluent primary cultured puppy aortic smooth muscle cells that had been sodium-loaded with monensin. In 26 paired assays of plasina from four pairs of dogs, cells incubated in the presence of plasma from hypertensive dogs had significantly reduced total (p< 0.01) and ouabain-sensitive (p< 0.001)86Rb+uptakes, but their intracellular sodium content did not differ from cells incubated in paired normotensive plasma. We no longer detected these uptake differences when passaged cells or cells cocultured with bovine endotheliaJ cells were used for assay or when plasma was treated with protease inhibitors or boiled. However, boiled plasma increased the sodium content of the assay cells, suggesting an ionophorelike effect. Levels of pump inhibitory activity in plasma appeared to remain constant during Weeks 1 to 6 of hypertension. We found no evidence for altered numbers of pump sites in cardiovascular tissues from these hypertensive dogs.'These findings support the hypothesis that plasma factors inhibit the membrane Na+-K+pump in vascular smooth muscle cells in this form of hypertension. These plasma inhibitory factors apparently do not induce pump molecules.

ISSN:0194-911X    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

The release of fatty acids from perfused mesenteries of spontaneously hypertensive rats (SHR) and control Wistar-Kyoto rats (WKY) was studied. The release of the prostaglandin precursors dihomogammalinolenic acid, arachidonte acid, and ekosapentaenoic acid was reduced in SHR when compared with age-matched WKY. The release of all other fatty acids detected in the effluent was also reduced. The differences in fatty add release were evident even when tissue levels of the fatty acids were similar or higher in SHR than in controls. The addition of evening primrose oil and fish oil into the diet partially corrected these defects. Evening primrose oil and fish oil both attentuated increases in blood pressure, but fish oil was more potent than primrose oil. Although both diets reduced vascular reactivity, primrose oil was more effective with lower doses of norepinephrine whereas fish oil blunted the effects of both low and high doses of norepinephrine. The possible mechanisms for the effects of primrose oil and fish oil on vascular reactivity are briefly discussed.

ISSN:0194-911X    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

The vascular wall has the capacity to produce thromboxane A2. However, the role of vascular thromboxane A2is still uncertain. In this study, we examined the relationship between vascular thromboxane A2generation and vascular smooth muscle cell growth in spontaneously hypertensive rats (SHR). Vascular thromboxane A2generation was significantly enhanced by 49% in 5-week-old and by 117% in 15-week-old SHR as compared with age-matched Wistar-Kyoto rats (WKY). Thromboxane A2generation was also significantly enhanced by 59% in the cultured vascular smooth muscle cells of SHR when compared with production in WKY. Vascular smooth muscle cells of SHR exhibited a significantly shortened doubling time (by 32%) and greater [3H]thymldlne uptake (by 56%), as compared with those of WKY. OKY 046 (10−5M), a thromboxane synthase inhibitor, significantly tempered the rapid vascular smooth muscle cell growth in SHR by 9% for doubling time and by 10% for [3H]thymidine uptake. OKY 046 did not Influence the doubling time of WKY. Conversely, a stable analogue of thromboxane A2dose-dependently stimulated the [3H]thymidine uptake by vascular smooth muscle cells of WKY, and, at a concentration of 10−5M, shortened the doubling time of vascular smooth muscle cells of WKY by 11%, whereas it showed slight effects on SHR. These data indicate that vascular thromboxane A2is involved in the regulatory mechanism of vascular smooth muscle cell growth and that enhanced vascular thromboxane A2generation is partly responsible for the rapid proliferation of vascular smooth muscle cells of SHR. The alterations of vascular thromboxane production may be a key trait for genetic hypertension.

ISSN:0194-911X    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

The sympathetic nervous system is an important factor that can induce increased renin secretion by the kidney. In recent years, the notion has arisen that the sympathetic nervous system may also function to set the level of responsiveness of the kidney to nonneural stimuli for renin secretion. However, evidence in favor of this possibility has come primarily from studies employing direct electrical stimulation of renal nerves, and no attempt has been made to determine if central neural sites can also influence the responsiveness of the kidney. In the present study, the ability of hypothalamic activation to enhance the renin response to suprarenal aortic occlusion was investigated. Conscious, freely moving rats with an inflatable cuff placed around the aorta were used to determine the relationship between renal perfusion pressure and plasma renin activity in the control state and during continuous low-level stimulation of the paraventricular nucleus. The stimulation resulted in a rightward shift in the curve that related renal perfusion pressure to plasma renin activity; that is, for any given decrease in renal perfusion pressure, the plasma renin activity was greater during the ongoing stimulation. This rightward shift appeared to be mediated by Increased renal nerve activity, since renal denervation prevented the shift. These data indicate that the hypothalamus, which plays an important role In regulating sympathetic activity, is capable of Increasing the sensitivity of the kidney to a nonneural stimulus for renin secretion. This effect may become important in certain hypertensive and prehypertensive states where central neural activity is thought to be enhanced.

ISSN:0194-911X    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

In a search for factors contributing to the sustained Mood pressure (BP) elevation in acutely volume-loaded animals, dextran dissolved in lactated Ringer's solution (20 ml/kg) was infused into 34 mongrel dogs over a period of 1 hour under pentobarbital anesthesia and changes in bemodynamic and humoral variables were monitored during its infusion and for 3 hours after its infusion. BP elevation during volume loading (from 114 ± 3 to 128 ± 3 [SEM] mm Hg) was attributed to an increase in cardiac output. After volume loading, some dogs maintained BP elevation whereas others did not. The former group showed an increase in total peripheral resistance, demonstrating a transformation of cardiac output to total peripheral resistance as a responsible factor in maintenance of the elevated BP. The plasma levels of norepinephrine, vasopressin, and plasma renin activity were not elevated, indicating that these vasoactive factors were not responsible for elevation of the BP or total peripheral resistance. The changes in the hematocrit, atrial natriuretk factor, urine volume, and urinary sodium excretion were identical in the two groups, and natrluresis was not prominent when total peripheral resistance was high. Pressor responses to norepinephrine and angiotensin II were potentiated 3 hours after stopping Infusion in both groups, but this potentiation was not correlated with the Increase in total peripheral resistance or mean BP. Thus, acute volume expansion produced resistance-dependent hypertension following the initial volume-dependent hypertension. It is unlikely that a vascular sensitizing natriuretk factor plays a role in the resistance-dependent BP elevation. The mechanism and physiological importance of hypersensitivity to vasoactive substances remain to be elucidated.

ISSN:0194-911X    

出版商:OVID    

年代:1988

数据来源: OVID