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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A review of findings pertaining to EDRF (endothelium derived relaxation factor) which proved to be nitric oxide, NO. After an account of the vasodilatating action of NO in the cardiovascular system the main attention is devoted to macrophages, the source of NO and to the formation of NO during activation of infections and during septic shock. NO participates also in the cytotoxicity of macrophages. NO may be the cause of hypotension in hepatic failure. Cumulation of endogenous inhibitors of NO formation in renal failure may be the cause of hypertension. The author analyzes other clinical effects of NO with regard to impotence and diabetes: NO stimulates insulin secretion from the B-cells of the islets of Langerhans. Attention is also drawn to the possible function of NO in the pituitary, in particular with regard to the arginine test which stimulates STH secretion.
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PMID:[A new agent--nitric oxide]. 148 81

An animal model was developed to study the pathophysiology of erectile dysfunction due to atherosclerotic vascular disease. Thirty one New Zealand white male rabbits were divided into control (n = 5) and treatment groups (n = 26). The control group was placed on a regular diet while the treatment group underwent balloon de-endothelialization of the aorto-iliac arteries and received 1.6% cholesterol and 4% triglyceride diet for eight weeks. After eight weeks in the control animals (n = 5), blood levels of cholesterol, triglycerides and low density lipoproteins, radiologic studies as well as hemodynamic parameters of erectile function were all normal. In the surviving treatment animals (n = 21) after the same time period, a significant increase in blood levels of cholesterol, triglyceride and low density lipoprotein were observed. In addition, 62% of these animals developed hypertension which was not observed in the control group. Angiographically, 10 animals (48%) demonstrated severe atherosclerotic lesions (75% to 100% occlusion of common or internal iliac arteries on one side and over 50% occlusion of the opposite side), five (24%) had moderate lesions (50 to 75% luminal occlusion of right and left common iliac or internal iliac arteries) and 6 revealed minimal lesions (less than 50% occlusion of the right and left common iliac or internal iliac arteries). Of the 15 animals with 50% or greater luminal occlusion of the iliohypogastric arteries, erectile dysfunction was found in 93% of cases. Due to the development of erectile dysfunction in 33% of animals with minimal occlusive lesions, it appears that factors, other than large vessel luminal occlusion, may exist in this animal model which adversely influence erectile function. This model may therefore be of further benefit in the study of other factors associated with atherosclerosis and impotence, such as the possible concomitant hypercholesterolemic and atherosclerotic-induced alterations in the local reactivity of corpus cavernosum smooth muscle and lacunar space endothelial cells.
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PMID:Erectile dysfunction due to atherosclerotic vascular disease: the development of an animal model. 159 19

The value of the vascular examination cannot be over-estimated. Symptoms of vascular disease present in the foot and lower extremity may actually be manifestations of severe life-threatening disease. Symptoms, their location, and the frequency and quality of the patient's pain often provide valuable clues for the clinician's diagnosis. Central nervous system symptoms, ocular disturbances, cardiac symptoms, impotence, or constitutional disturbances may all indicate systemic arterial disease. Risk factors for this disease include smoking, hypertension, hyperlipidemia, genetic predisposition, diabetes, emotional stress, and physical inactivity. Those factors attributable to hypercoagulability and venous disease are birth control pill use, estrogen chemotherapy, obesity, prolonged immobilization, paralysis, previous thrombotic episodes, venous stasis disease, and varicose veins. An accurate bilateral assessment of blood pressure, pulses, and capillary perfusion is of critical importance. Careful inspection of the extremity for trophic changes, skin color, texture, temperature, edema, ulceration, atrophy, or paresis, will provide clues of vasculopathy. A relatively accurate assessment of circulatory status may be obtained without the use of exotic instruments. Simple tests such as the elevation and dependency tests, capillary bed return test, venous filling time test, along with blood pressure, pulse, and possibly oscillometry data are valuable in arterial evaluation. Such venous tests as inspection, percussion, Homan's sign, Trendelenburg, and Perthes' tourniquet are useful in the determination of the presence of venous disease. Fortunately, over the past few years tremendous advances have been made in the technology of the vascular laboratory. If symptoms are discovered during the vascular history and physical examination, the complete noninvasive study will provide impressive data to quantitate and specifically establish the diagnosis.
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PMID:The vascular history and physical examination. 173 54

The most common cause of death in hypertensive patients is myocardial infarction (MI), being three times more common than stroke. Lowering raised BP results in 40% fewer strokes, but only 14% fewer MIs. This may be because other coronary risk factors that often accompany hypertension (e.g. obesity, lipid and thrombotic disturbances, insulin insensitivity, increased plasma renin activity and increased sympathetic activity) are either unaffected or exacerbated by some of the traditional antihypertensive agents. Some of these risk factors show a diurnal rhythm peaking at 07.00-10.00 hours, thus this time constitutes a 'vulnerable period' for sudden death or death from MI. beta-blockers and diuretics have been effective in preventing stroke, but diuretics (at least potassium-losing diuretics) might actually increase the incidence of sudden death and MI in young to middle-aged hypertensive subjects (though elderly patients may benefit). Quality of life can be impaired by some beta-blockers, and diuretics can cause metabolic upset and male impotence. Thus, antihypertensive agents that are not only effective and well tolerated but are beneficial to the broader coronary risk profile are desirable. ACE inhibitors should prove particularly useful in terms of: good quality of life; non-exacerbation or improvement of coronary risk factors; treating patients with impaired left ventricular function; reversing left ventricular hypertrophy and vascular wall hypertrophy, thus improving coronary flow reserve; atheroma regression; renal protection, particularly in diabetes; and prevention or regression of LV dilatation (remodelling) following MI.
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PMID:What does the future hold for ACE inhibitors? 179 18

Sexual impotence is the main andrological complication of diabetes mellitus and is the consequence of nervous, vascular and psychological factors which act either separately or in association. An attempt to prevent this complication will be successful if performed early before impotence has became irreversible. Neuropathy-induced impotence can be prevented by obtaining a good metabolic control of diabetes and/or by using some specific drugs such as gangliosides and aldose reductase inhibitors. The vascular causes of erectile failure can be prevented by reducing or removing associated risk factors such as smoking, hypertension, obesity, hypercholesterolemia, sedentariness and insulin-resistance. Finally, correct information and reassurance of the patient and his partner can prevent the negative role played by psychological factors on the sexual dysfunctions complained by the diabetic subject.
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PMID:[Is it possible to prevent andrological complications in the diabetic patient?]. 183 28

A total of 132 consecutive patients with erectile impotence underwent extensive evaluation, including vascular evaluation with intracavernous injection of papaverine and penile duplex ultrasonography, to determine the etiology of impotence. Three vascular risk factors, smoking, diabetes mellitus and hypertension, were investigated for their impact on vasculogenic impotence. The patients were divided into four groups: one with no risk factors, one with one vascular risk factor, one with two vascular risk factors, and one with all three risk factors. The results of penile vascular evaluation in these patient groups were compared. The incidence of penile vascular impairment was found to be higher in patients with one vascular risk factor than in those with none. The proportion of abnormal penile vascular findings significantly increased as the number of risk factors increased. These data confirm the important role of vascular risk factors, smoking, diabetes mellitus, and hypertension, in the pathogenesis of organic impotence.
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PMID:Cigarette smoking and other vascular risk factors in vasculogenic impotence. 188 36

To determine whether impotence is caused by specific and consistent changes in erectile tissue, we compared the ultrastructure of the corpora cavernosa in 6 controls with that in 59 patients undergoing implantation of a penile prosthesis. The impotent patients were divided into groups based on a medical history of hypertension (10), pelvic surgery (9), alcoholic smokers (8), hypertensive alcoholics (3), hypertensive alcoholic smokers (3), smokers (3), diabetics (8), diabetic smokers (3), Peyronie's disease (3), spinal cord injury (3) and isolated causes (6). Our data demonstrate that different behavioral and/or medical conditions produce similar degenerative tissue responses. There is no single or specific cause of impotence that is manifest by consistent changes in erectile tissue.
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PMID:Ultrastructural changes in impotent penile tissue: a comparison of 65 patients. 200 94

We investigated the relationship between cigarette smoking and atherosclerosis of the hypogastric-cavernous arterial bed by evaluating arteriograms of young impotent men referred for selective pudendal angiography. Those patients with hemodynamically significant atherosclerosis had smoked more pack-years than had patients without arterial disease. These differences were statistically significant (p less than 0.05) for the common penile artery (32.8 pack-years, 40 patients versus 22.3 pack-years 57 patients) and the dorsal artery (31.3 pack-years, 48 patients versus 22.0 pack-years, 49 patients). The effect of cigarette smoking as an independent risk factor for atherosclerotic disease in the hypogastric-cavernous arterial bed was evaluated as well. When controlled for age, trauma history, hypertension and diabetes, cigarette smoking was independently associated with atherosclerosis in the internal pudendal artery (p less than 0.05). The relative risk (and 95% confidence interval) of developing internal pudendal artery atherosclerosis for each 10 pack-years smoked was 1.31 (1.05 to 1.64). A third analysis investigated the potential interactive effects of cigarette smoking and pelvic or perineal trauma. A significantly higher incidence (p less than 0.05) of cavernous artery atherosclerosis was found among smokers with a history of chronic perineal trauma (33 patients) compared to nonsmokers with a similar history (25 patients). The findings of this study indicate that cigarette smoking is an independent risk factor in the development of atherosclerotic lesions in the internal pudendal and common penile arteries of young impotent men. Cigarette smoking appears to predispose these patients to early atherosclerotic lesions in the cavernous artery following chronic perineal trauma.
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PMID:Cigarette smoking: an independent risk factor for atherosclerosis in the hypogastric-cavernous arterial bed of men with arteriogenic impotence. 200 95

In a group of 472 impotent patients who were evaluated with pharmacologic duplex sonography, 117 patient (24.8%) had a history of hypertension, 26 of them (22.2%) for more than 10 years. Objective data about the changes in pulsation, diameter and blood flow velocity of the penile arteries after papaverine injection and the resulting erectile response allowed indirect assessment of the penile venous function. Varying degrees of impaired arterial function were diagnosed in 85% of the patients. The duration of hypertension had less deteriorating effects on the penile arterial system than second risk factors such as diabetes mellitus (n = 31) or smoking (n = 26). Patients on antihypertensive medication (n = 88, 75.2%) demonstrated a worse arterial response to papaverine than those without medication (n = 29, 24.8%). The best vascular response to papaverine injection was found in patients taking a combination of beta-blockers and vasodilators (n = 6), whereas thiazides either taken alone or in combination (n = 51, 60%) seem to have a deteriorating effect on arterial function. However, the arterial response did not correlate with the ability to achieve 'full erection' after intracavernous papaverine injection. Clinical experience confirms that certain antihypertensive drugs affect not only the blood pressure, but also compliance of the erectile tissue resulting in a functional venous leak. This may impair erectile function as much as arteriosclerotic changes of the vascular system secondary to hypertension.
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PMID:Hypertension and impotence. 200 14

The majority of cases of impotence are associated with vascular risk factors such as diabetes, hypercholesterolemia, hypertension and smoking. These factors induce impairment of endothelium-dependent relaxation of blood vessels in man and in experimental animals. In this study the effects of hypercholesterolemia on the reactivity of rabbit corpus cavernosum smooth muscle strips to endothelium-dependent and endothelium-independent agents were investigated. New Zealand White rabbits (n = 14) were randomly divided into control and treatment groups. The control group (n = 7) received a regular diet while the treatment group (n = 7) was fed a diet of 0.5% cholesterol and 4% peanut oil for 10 weeks. Animals were then sacrificed and the corporal tissue studied in organ chambers for isometric tension measurement. Tissue was contracted with phenylephrine and concentration-dependent relaxation to acetylcholine, in the presence and absence of indomethacin, and to nitroprusside were examined. Blood level of cholesterol in the cholesterol-fed group was significantly higher compared to the control group. Contractions to phenylephrine were similar in both groups. Hypercholesterolemia, however, inhibited relaxation to acetylcholine but did not alter relaxation to nitroprusside, a cyclic guanosine monophosphate (cGMP)-dependent, direct smooth muscle dilator. Indomethacin enhanced the relaxations to acetylcholine in both control and cholesterol-fed groups but did not correct the difference in the relaxation to acetylcholine between both groups. It is concluded that hypercholesterolemia impairs endothelium-mediated relaxation of rabbit corpus cavernosum smooth muscle. The mechanism for the endothelial dysfunction does not appear to involve alteration in cyclooxygenase products of arachidonate or the cGMP-dependent relaxation of corporal smooth muscle. Impairment of endothelium-dependent relaxation of corporal smooth muscle may contribute to the pathophysiology of impotence associated with hypercholesterolemia in man.
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PMID:Hypercholesterolemia impairs endothelium-dependent relaxation of rabbit corpus cavernosum smooth muscle. 205 97


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