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

The binding of tritiated ligands for various opiate receptor subtypes to brain membranes prepared from spontaneously hypertensive rats and normotensive Wistar-Kyoto rats was determined. The density (Bmax) or the apparent dissociation constant (Kd) for the binding of the mu-ligand (naltrexone) and delta-ligand (Tyr-D-Ser-Gly-Phe-Leu-Thr) to brain membranes of hypertensive and normotensive rats did not differ. However, the Bmax for the binding of kappa-ligand (ethylketocyclazocine, EKC) to brain membranes after the suppression of mu and delta-sites by 100 nM each of unlabeled D-Ala2-MePhe4-Gly-ol5-enkephalin and D-Ala2-D-Leu5-enkephalin, respectively, was significantly greater in hypertensive rats compared to normotensive rats. The Kd values for the binding of 3H-EKC in the two groups did not differ. The binding of 3H-EKC in brain regions was in the order: hypothalamus greater than midbrain greater than striatum greater than cortex greater than pons + medulla. The increase in the binding of 3H-EKC in the brain of hypertensive rats compared to normotensive rats was due to increased binding in the hypothalamus and cortex. These results provide for the first time evidence of selective proliferation of kappa-opiate receptors in the brain of hypertensive rats, and suggest that brain kappa-opiate receptors may play an important role in the pathophysiology of hypertension.
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PMID:Selective proliferation of brain kappa opiate receptors in spontaneously hypertensive rats. 302 39

Mammalian atria have previously been shown to produce a variety of peptides with natriuretic and vasorelaxant activities. Certain of these atrial natriuretic factors (ANF) have been localized immunocytochemically in secretory granules of atrial myocytes. However, the precise sites of action and extra-atrial synthesis or accumulation of ANF have not been identified immunocytochemically. In the present study, immunoreactive ANF was detected in rat atrial myocytes, intercalated cells of the renal collecting ducts, adrenal medullary chromaffin cells, and gonadotrophs of the anterior pituitary using an antibody against synthetic rat ANF-IV (H2N-Arg-Ser-Ser-Cys-Phe-Gly- Gly-Arg-Ile-Asp-Arg-Ile-Gly-Ala-Gln-Ser-Gly-Leu-Gly-Cys-Asn-Ser-Phe- Arg-Try-COOH). The localization of ANF in specialized cells of the renal collecting tubules and ducts supports suggestions that these structures may be a site of natriuretic action of ANF. In addition, immunocytochemical localization of ANF in the rat adrenal medulla and anterior pituitary suggests the existence of alternate sites of action and/or synthesis. We believe these findings are important for a more complete understanding of the role of ANF in fluid and sodium regulation and of the participation of ANF in the development of sodium-dependent hypertension.
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PMID:Immunocytochemical localization of atrial natriuretic factor in the kidney, adrenal medulla, pituitary, and atrium of rat. 316 Jul 63

The successful treatment of a patient who developed the TUR syndrome is described. Glycine 2.2% in water was used as irrigating fluid. Initial symptoms were visual disturbances and hypertension. Repeated blood chemistry analyses revealed elevations in the serum concentrations of most non-essential amino acids. Later on the patient experienced vivid hallucinations.
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PMID:Hallucination and visual disturbances in transurethral prostatic resection. 318 95

Hypertension-induced renal damage is mediated by increased glomerular pressure and flow. These alterations have been evaluated by the renal response to protein or amino acids. To test this assumption, we studied glomerular hemodynamic responses to glycine infusion in rats with reduced renal mass, with and without Goldblatt hypertension. The left kidney was ablated by two thirds in 12 rats, and in 5, hypertension was induced by clipping the right renal artery. Seven normal, unmanipulated rats served as controls. Micropuncture was performed in the left kidney during control and 15% glycine infusion periods, 45 days after surgery. Arterial pressure was higher in hypertensive rats (160.3 mm Hg) than in controls (103.8 mm Hg) and rats with renal ablation (125 mm Hg; p less than 0.05). Higher values of single-nephron glomerular filtration rate and single-nephron plasma flow in rats with renal ablation (63.0, 223.7 nl/min) and hypertension (46.1, 239.7 nl/min) than in controls (28.8, 94.9; p less than 0.05) demonstrated the presence of hyperfiltration. However, glomerular pressure was elevated only in hypertensive rats (40.1 mm Hg), when compared to controls (32.7 mm Hg; p less than 0.05) and rats with renal ablation (33.4 mm Hg; p less than 0.05). Glycine increased single-nephron glomerular filtration rate and single-nephron plasma flow in control rats by 76 and 65%; rats with renal ablation had only partial responses, 35% and 23%, respectively, whereas in hypertensive rats the response was completely abolished. Glycine detected hyperfiltration and unmasked a dysfunction of preglomerular vessels that was greater in hypertensive rats and could contribute to the rise in glomerular pressure and flow and thereby to glomerular damage.
Hypertension 1988 Feb
PMID:Evaluating hyperfiltration with glycine in hypertensive rats with renal ablation. 334 63

The purpose of these experiments was to investigate whether the vasodilator tissue hormone bradykinin contributes to the maintenance of normal blood pressure. A newly synthesized peptide competitive antagonist of bradykinin, the compound Arg-Pro-Hyp-Gly-Phe-Ser-DPhe-Phe-Arg-trifluoracetic acid (B3852), capable of inhibiting the depressor effect of exogenous bradykinin by over 50%, was infused into 10 normotensive rats at a rate of 500 micrograms/0.1 ml/min. Blood pressure rose immediately, from a baseline of 104 +/- 5 to 131 +/- 7 mm Hg at the end of a 5-minute infusion, and returned to baseline within 2 to 3 minutes after discontinuation of the infusion. When similar doses were administered by continuous infusion to previously nephrectomized rats (n = 5) or as an acute bolus to adrenalectomized rats (n = 5), blood pressure rose from 111 +/- 3 to 125 +/- 5 mm Hg and from 112 +/- 4 to 128 +/- 5 mm Hg, respectively. The data suggest that a vasodepressor action of endogenous bradykinin contributes to maintenance of normal peripheral vascular tone, and that this action is not mediated through adrenal catecholamines or renomedullary prostaglandins.
Hypertension 1987 Jun
PMID:Contribution of bradykinin to maintenance of normal blood pressure. 359 81

We have studied inhibition of homogeneous human converting enzyme by a new inhibitor, a ketomethylene derivative of the blocked tripeptide substrate, Bz-Phe-Gly-Pro (ketoACE). KetoACE inhibited the hydrolysis of Hip-His-Leu and Hip-Phe-Arg at different concentrations (I50 values were 4 X 10(-8) M and 2 X 10(-7) M, respectively). Kinetic studies indicated that ketoACE inhibits the hydrolysis of both substrates by a similar, non-competitive mechanism. At the lowest enzyme concentration tested, using 3H-Hip-Gly-Gly as substrate, the I50 of ketoACE was 6 X 10(-9) M. KetoACE protected a functional tyrosine residue in the active site of human converting enzyme from modification with N-acetylimidazole. It is proposed that there are alternate (hydrophobic) binding sites for both inhibitors and substrates in the active site of human converting enzyme. It should be possible to develop other high-affinity inhibitors of this class that bind to hydrophobic sites and do not require metal binding via a sulfhydryl group.
Hypertension
PMID:Inhibition of human converting enzyme in vitro by a novel tripeptide analog. 626 59

Spontaneously hypertensive rats exhibited dopamine receptor supersensitivity as evidenced by a greater hypothermic response to apomorphine in comparison with normotensive Wistar-Kyoto rats. A single injection of cyclo(Leu-Gly) given prior to apomorphine administration did no alter apomorphine induced hypothermia in either the normotensive or the hypertensive rats. Chronic administration of cyclo(Leu-Gly) for 7 days did not affect apomorphine response in normotensive rats, but blocked the exaggerated response to apomorphine in the hypertensive rats. These studies suggest that cyclo(Leu-Gly) interacts with the dopamine receptors and that the central dopamine receptors may play a role in the pathophysiology of hypertension.
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PMID:Effect of cyclo(Leu-Gly) on the supersensitivity of dopamine receptors in spontaneously hypertensive rats. 684 87

A shortened and modified eledoisin-hexapeptide sequence (Lys-Phe-Ile-Gly-Leu-MetNH2) was tested for their action on avoidance learning and blood pressure of rats with spontaneous hypertension (SH-rats) and intact Wistar rats. Both groups were 10, 14, and 26 weeks of age. Disorders of avoidance learning and elevation of blood pressure were likely to aggravate along with growing age of SH-rat. The used eledoisin-hexapeptide sequence is related to the essential C-terminal pentapeptide sequence of Substance P (SP). After injection of the used hexapeptide at doses of 250 microgram/kg intraperitoneally disorders in avoidance learning were completely eliminated from ten-week SH-rats or conditionally for SH-rats aged 14 and 26 weeks. Elevated blood pressure in SH-rats aged 26 weeks was reduced by the hexapeptide from 220 Torr to approximately 190 Torr. Blood pressure in SH-rats aged 14 weeks, originally about 180 Torr, was almost unaffected by the hexapeptide. Blood pressure went up from about 150 Torr to 190 in ten-week-old Sh-rats. A hypothesis was made about the mode of action of Substance P and related peptides.
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PMID:Effects of a substance P-analogue on blood pressure and avoidance learning of rats with spontaneous hypertension. 728 83

We evaluated signs and symptoms of the transurethral resection syndrome recorded during and after 273 transurethral prostatic resections performed at 2 hospitals between 1984 and 1993. Glycine solution was used as the irrigant and ethanol served as a tracer for fluid absorption. The incidence and severity of symptoms that could possibly be related to the syndrome increased progressively as more glycine solution was absorbed. Patients who absorbed 0 to 300 ml. of glycine solution had an average of 1.3 such symptoms. This number increased to 2.3 when 1,001 to 2,000 ml. were absorbed, 3.1 when 2,001 to 3,000 ml. were absorbed and 5.8 for volumes greater than 3,000 ml. Nausea and vomiting occurred significantly more often when 1,001 to 2,000 ml. were absorbed compared to no absorption. Confusion and arterial hypotension were other prominent signs of fluid absorption, whereas hypertension was not. The severity of symptoms was markedly aggravated when more than 3,000 ml. were absorbed. Extravasation resulted in higher risks of bradycardia, hypotension and failed spontaneous diuresis postoperatively than absorption by the intravascular route.
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PMID:Symptoms of the transurethral resection syndrome using glycine as the irrigant. 753 56

A point mutation in the apolipoprotein AI (apoAI) gene causing autosomal dominant non-neuropathic systemic amyloidosis is described in a previously unreported Canadian family of British origin with five affected individuals in three generations. Amyloid deposits in the renal biopsy from the proband, a 31-year-old female presenting with hypertension and renal failure, stained immunospecifically with antiserum to apoAI. The plasma of all family members with amyloidosis contained both wild-type apoAI and a variant bearing one additional positive charge. Sequencing of the apoAI gene demonstrated that the proband was a heterozygote for a single base substitution in exon 3, changing codon 26 from GGC(Gly) to CGC(Arg). Concordance of the mutant allele with the presence of variant plasma apoAI and clinical features of amyloidosis was demonstrated. This is the third family in which this amyloidotic mutation has been described, but the distribution of amyloid deposits and their clinical effects are clearly determined by other genetic and/or environmental factors.
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PMID:Familial nephropathic systemic amyloidosis caused by apolipoprotein AI variant Arg26. 820 2


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