Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this review, we examine the changes in sexual function that accompany deviations from "normal" physiological states. We propose that the changes one observes in many altered physiological states should not be viewed in isolation. We describe our paradigms for assessing sexual function, and proceed to evaluate how sexual function changes with hormonal deprivation and aging, in rat models for hypertension, in severe hyperprolactinemia, in streptozotocin-induced diabetes, after chronic alcohol intake, after chronic morphine administration, and after exposure to the heavy metal, cadmium. We will provide evidence for the involvement of adrenergic transmitters and two neuropeptides, neuropeptide Y and somatostatin, in the neuroendocrine regulation of sexual behavior. Finally, we compare and contrast the changes observed relative to the changes seen in "normal" aging in rats. The sequence of age-related changes in sexual function is distinct. The first change observed is a decrement in ex copula erectile reflexes. Next are decreases in ejaculatory threshold, followed shortly by increases in initiation and reinitiation of copulation after ejaculation. This is followed by a decrement in the number of males copulating to ejaculation. Finally, there is a failure to initiate the copulatory process. This sequelae is relatively common, being evident after castration, with hyperprolactinemia, and after exposure to cadmium. The data available for sexual function in hypertension is incomplete and modified by the etiology, but a suggestion for this sequelae is seen in SHR. In contrast, sexual dysfunction associated with chronic morphine administration appears to be due to an initial deficit in motivational aspects. Testosterone reverses sexual dysfunction associated with castration, but not with idiopathic sexual inactivity, nor with sexual dysfunction associated with aging, diabetes, or chronic morphine administration. Comparing sexual function in rat models for hypertension, diabetes and chronic ethanol leads to the conclusion that increases in blood pressure, like decreases in testosterone, cannot be the primary causal factor for sexual dysfunction. Age, hormonal history of the subject, and the age at castration influence changes in sexual function. Age-related sexual dysfunction appears to be contributed to by changes in adrenergic-neuropeptidergic, to include sympathetic, systems. Site-specific administration of NPY induces alterations in parameters of copulatory behavior which mimic those seen in aging and the retention of ejaculatory behavior with aging is associated with site-selective attenuation (or reversal) of age-associated changes in NPY content. Yohimbine enhances copulatory activity in castrated and aging rats, and attenuates or reverses the antisexual effects of clonidine, epinephrine and somatostatin.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Sexual function in altered physiological states: comparison of effects of hypertension, diabetes, hyperprolactinemia, and others to "normal" aging in male rats. 763 May 83

To study the relationship between somatostatin (SS), atrial natriuretic peptide (ANP), beta-endorphin (beta-EP), aldosterone (Aldo) and pregnancy induced hypertension (PIH), blood was collected from 69 cases, including non-pregnant women, normal pregnant women, patients with PIH and their newborns (umbilical arteries) and plasma levels of ANP, SS, beta-EP, Aldo were measured by radioimmunoassay. Results indicated that ANP, SS beta-EP and Aldo levels either during normal pregnancy or at delivery were significantly higher than those in non-pregnant women. ANP, SS and beta-EP levels in last trimester of patients with PIH, particular in severe cases, were significantly higher than those in normal pregnancy or moderate PIH whereas Aldo levels were lower in PIH when compared with normal pregnancy. A positive correlation between ANP, SS levels and the severity of PIH was observed. Levels of ANP, SS, beta-EP and Aldo in newborns were higher than those in mothers at delivery. Levels of ANP and SS in neonates born to mother of PIH were much higher, whereas beta-EP and Aldo were lower as compared with normal pregnancy. The conclusion is that high levels of ANP and Aldo during pregnancy may play an important role in stabilizing blood pressure and maintaining the balance of water and electrolyte. Therefore it could be used as an index for prediction of PIH.
 ...
PMID:[Relation between somatostatin, atrial natriuretic peptide, beta-endorphin, aldosterone and pregnancy induced hypertension]. 790 29

The purpose of this study was to examine whether impaired insulin clearance contributes to the hyperinsulinemia observed in humans with essential hypertension. Previous studies from our group and others have demonstrated that individuals with essential hypertension are resistant to the glucoregulatory effect of insulin. Animal models have confirmed this finding and have suggested that hypertensive animals have impaired insulin clearance that might contribute to the observed hyperinsulinemia. The metabolic clearance rate of insulin (MCRins) was calculated during a constant infusion of glucose (320 mg/m2/min) and insulin (25 mU/m2/min), under conditions where endogenous insulin secretion was suppressed by somatostatin infusion (250 micrograms/h) for four groups of age sex and weight-matched patients: normotensive volunteers, untreated hypertensives, hypertensives treated with diuretics and hypertensives treated with diuretics and beta-blockers. MCRins was impaired in all three groups of hypertensive subjects compared with normal BP volunteers, particularly in untreated hypertensives and those treated with combination diuretic and beta-blocker therapy: normal = 0.6 +/- 0.1; untreated = 0.47 +/- 0.2; diuretic = 0.51 +/- 0.1; combination = 0.39 +/- 0.2 (in ml/min, expressed as mean +/- SD). The effectiveness of somatostatin for islet suppression was confirmed by demonstrating markedly diminished C-peptide concentrations in untreated hypertensives and normal volunteers. Thus, our previous finding of elevated steady-state plasma insulin during insulin suppression testing in hypertensives seems not to be the result of impaired pancreatic response to somatostatin but, rather, there seems to be a defect in insulin clearance in these individuals not unlike that demonstrated in animal models of hypertension and insulin resistance. The nature of this defect remains to be elucidated.
 ...
PMID:Impaired insulin clearance in essential hypertension. 791 38

In the severe crisis of carcinoid syndrome the flush is usually accompanied by hypotension and occasionally shock. Injection of octreotide, the long-acting analog of somatostatin, usually prevents or aborts this vasomotor reaction. A small minority of carcinoid syndrome patients manifest hypertension during their crises and little has been reported in the literature on their management. We present the first case reports of the response of patients with hypertensive carcinoid crisis to treatment with octreotide. The world literature contains reports of 20 prior cases of hypertensive carcinoid crises occurring in association with the stress of surgery and anesthesia. Review of these cases reveals no common feature, other than hypertension, that might clearly distinguish them from the typical hypotensive carcinoid syndrome patient. It is hypothesized that the mechanism of action of octreotide correcting the blood pressure changes in all carcinoid crises is via its known inhibition of vasomotor product release from the tumor and blocking receptors for these substances. We suggest that hypertensive as well as hypotensive carcinoid crises respond to octreotide and that this agent should be considered for prophylactic and emergency use in all carcinoid syndrome patients prior to and during anesthesia and surgery.
 ...
PMID:Octreotide treatment of carcinoid hypertensive crisis. 796 29

Resistance to insulin-mediated glucose disposal has been previously shown to be increased in association with obesity, high blood pressure, and non-insulin-dependent diabetes mellitus. We initiated the present study to quantify the separate effects of hypertension and non-insulin-dependent diabetes mellitus on insulin resistance in both nonobese and obese subjects. To accomplish this, 88 subjects were divided into the following five experimental groups: normal blood pressure, nonobese (n = 17); normal blood pressure, obese (n = 18); high blood pressure, nonobese (n = 18); high blood pressure, obese (n = 19); and high blood pressure, obese, non-insulin-dependent diabetes mellitus (n = 16). Plasma glucose and insulin concentrations were measured before and after a 75-g oral glucose load. Resistance to insulin-mediated glucose disposal was estimated by determining the steady-state plasma insulin and glucose concentrations during the last 30 minutes of a continuous infusion of somatostatin (5 micrograms/min), exogenous insulin (25 mU/m2 per minute), and glucose (240 mg/m2 per minute). Since the steady-state plasma insulin concentrations are similar in all subjects, the higher the steady-state plasma glucose, the more insulin resistant the individual. Nonobese subjects with normal blood pressure had the lowest plasma glucose and insulin responses and steady-state plasma glucose concentrations, and their values were significantly different from the other four groups. Obese or nonobese subjects with high blood pressure had significantly higher plasma glucose responses and steady-state plasma glucose concentrations than did their respective weight-matched control subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1994 Dec
PMID:Additive effects of obesity, hypertension, and type 2 diabetes on insulin resistance. 799 25

Neuropeptides are ubiquitous in the sympathetic system and modulate transmission at the levels of the intermediolateral cell column, sympathetic ganglia, and neuroeffector junctions. Several neuropeptide-containing pathways from the hypothalamus and medulla modulate excitability of preganglionic neurons. Neuropeptides coexist with norepinephrine or acetylcholine in subpopulations of chemically coded, target-specific sympathetic ganglion neurons. Neuropeptide Y is colocalized in adrenergic vasoconstrictor neurons, whereas vasoactive intestinal polypeptide is colocalized in cholinergic sudomotor neurons. Neuropeptide expression is plastic; during development, neurons that switch from a noradrenergic to a cholinergic phenotype increase expression of vasoactive intestinal polypeptide, somatostatin, and substance P. Preganglionic inputs increase neuropeptide Y and inhibit substance P expression. Sympathetic denervation produces sprouting of sensory fibers containing substance P and calcitonin gene-related peptide in target tissues. Neuropeptides from preganglionic fibers (e.g., enkephalin) and primary afferents (e.g., substance P, vasoactive intestinal polypeptide) modulate transmission in sympathetic ganglia. Neuropeptide Y produces vasoconstriction, prejunctional inhibition of norepinephrine release, and postjunctional potentiation of norepinephrine effects. Plasma neuropeptide Y increases during intense sympathoexcitation, hypertension, and pheochromocytoma. Dystrophic neurites containing neuropeptide Y occur in human sympathetic ganglia during aging, diabetes, and dysautonomia. Sympathetic neuropeptides may thus have important clinical implications.
 ...
PMID:Neuropeptides in the sympathetic system: presence, plasticity, modulation, and implications. 802 63

To determine whether insulin resistance and hyperinsulinemia are causally related to fructose-induced hypertension, we used vanadyl sulfate, a drug that improves insulin sensitivity in rats. Chronic oral vanadyl treatment was initiated in 6-week-old male Sprague-Dawley rats. One week after vanadyl was started, rats were fed either normal rat chow or a fructose-enriched diet. Plasma glucose and insulin levels and systolic blood pressure were measured weekly for 4 weeks. Fructose feeding induced hyperinsulinemia (fructose-fed, 366.6 +/- 8.4 versus control, 276 +/- 10.8 pmol/L, P < .001) and increased blood pressure (fructose-fed, 160 +/- 3.0 versus control, 124 +/- 3.0 mm Hg, P < .001). Vanadyl (0.4 to 0.6 mmol/kg per day) prevented the rise in plasma insulin (treated, 211.2 +/- 6.0 pmol/L, P < .001) and blood pressure (treated, 127 +/- 3.0 mm Hg, P < .001) in the fructose-fed rats without a change in plasma glucose. No change in blood pressure was seen in the control group. After 4 weeks, euglycemic clamps were performed on 20-hour fasted, conscious, mobile rats. Low-dose porcine insulin infusion (14 pmol/kg per minute) with concomitant somatostatin infusion resulted in similar steady-state plasma glucose and insulin levels in the various groups. Hepatic glucose production was suppressed and similar among various groups under clamp conditions. Insulin sensitivity index (micromoles of glucose per kilogram per hour per picomole per liter of insulin) was reduced in the fructose-fed rats compared with controls (fructose-fed, 0.9 +/- 0.4 versus control, 5.4 +/- 1.2, P < .002).(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1994 Mar
PMID:Vanadyl sulfate prevents fructose-induced hyperinsulinemia and hypertension in rats. 812 55

1. The hypothesis that adrenocorticotrophin (ACTH)-induced hypertension is a consequence of steroid-induced hyperinsulinaemia was tested using the somatostatin analogue (sandostatin, octreotide) to inhibit insulin release in Sprague-Dawley (SD) rats (n = 41). 2. Octreotide (20 micrograms, twice daily) did not modify blood pressure, plasma glucose, bodyweight, water and electrolyte balance, or organ weights but inhibited insulin secretion in the SD rat. 3. Compared with sham injection, ACTH-treated (0.5 mg/kg per day) SD rats showed an increase in blood pressure (sham 111 +/- 4 mmHg; ACTH 140 +/- 5 mmHg on treatment day 10 (P < 0.01), organ weights, water intake, urine volume, plasma glucose, insulin and sodium concentrations, and decrease of bodyweight and plasma potassium concentration. 4. Systolic blood pressure in rats treated with combined octreotide and ACTH was similar to that in rats on ACTH alone. Plasma insulin concentration was lower in octreotide + ACTH treated rats than with ACTH treatment alone. There were no differences in body or organ weights, plasma glucose, water or electrolyte balance. 5. Octreotide lowered plasma insulin concentration to the normal range but did not modify ACTH-induced hypertension in SD rats. These data do not support the notion that insulin-mediated alterations in blood pressure are a major mechanism for ACTH-induced hypertension in the rat.
 ...
PMID:Influence of somatostatin analogue (SMS 201-995, octreotide) on blood pressure in adrenocorticotrophin (ACTH) treated rats: role of hyperinsulinaemia in ACTH hypertension. 826 60

Glomerular hyperfiltration is a characteristic feature of acromegaly but it is uncertain whether albuminuria is elevated in this disease. To investigate the role of abnormal growth hormone (GH) and insulin-like growth factor I (IGF-I) levels on urinary protein excretion, we measured the overnight urinary albumin excretion rate (UalbV) and creatinine clearance in 14 acromegalic patients with metabolically active disease (fasting GH > 5 micrograms/l and IGF-I > 2.2 kU/l), 8 GH-deficient patients and 20 control subjects. The UalbV was higher in the acromegalic patients (median 8.4 (range 4.2-68.2) micrograms/min) than in the GH-deficient patients (2.0 (0.9-5.9) micrograms/min, p < 0.001) and control subjects (3.3 (1.0-7.8) micrograms/min, p < 0.01). Five acromegalic patients had UalbV levels above the normal upper normal limit of 10 micrograms/min. Only one patient with concomitant untreated hypertension had persistent microalbuminuria. Creatinine clearance also was higher in the acromegalic patients (p < 0.05) and lower in the GH-deficient patients (p < 0.05) than in the control subjects. In 11 of these acromegalic cases, the lowering of GH by 63% and of IGF-I by 48%, following treatment with the somatostatin analogue (N = 10) or spontaneous pituitary infarction (N = 1), reduced the UalbV by 29% to 4.9 (3.1-45.2) micrograms/min (p < 0.01). Among the acromegalic patients (25 observations), the UalbV was related to GH (r = 0.61, p < 0.01), IGF-I (r = 0.57, p < 0.01) and creatinine clearance (r = 0.54, p < 0.01). In conclusion, circulatory GH and IGF-I levels influence albuminuria.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Effect of growth hormone and insulin-like growth factor I on urinary albumin excretion: studies in acromegaly and growth hormone deficiency. 837

Pituitary tumours result in hypersecretion of different hormones which can be used in diagnosis. Prolactinomas can be diagnosed by measurement of prolactin serum concentration. Prolactin concentrations of > 150 to 200 micrograms/l are invariably due to macroprolactinoma. Lower levels may indicate microprolactinoma or a peripituitary tumour. Computed tomography scans visualize (micro)prolactinomas of 3 mm. Diagnosis of acromegaly is now based on measurement of serum IGF-I concentration. IGF-I levels correlate with the old test which measured insufficient suppression of GH levels to < 2 micrograms/l in response to oral glucose load. Most endocrine tumours have somatostatin receptors, allowing visualization with radiolabelled somatostatin analogues. 111In-diethylenetriaminopentaacetic acid-octreotide allows normal pituitary and somatostatin positive tumours to be visualized. A positive scan is predictive of good response to octreotide therapy. Cushing's syndrome is diagnosed by ecchymoses, myopathy, hypertension, and by measurement of the overnight 1 mg dexamethasone suppression test, urine cortisol levels and the diurnal cortisol rhythm. Clinically nonfunctioning macroadenomas in post-menopausal women often do not immunostain for gonadotropins. Serum gonadotropin levels are not elevated, although they do release gonadotropins or subunits in vitro. Diagnosis is assisted by TRH administration which increases serum gonadotropins or subunits, especially LH-beta.
 ...
PMID:Current tools in the diagnosis of pituitary tumours. 837 8


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>