A novel platelet-derived renal vasoconstrictor agent in normotensives and essential hypertensives

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A novel platelet-derived renal vasoconstrictor agent in normotensives and essential hypertensives. / Agha, A; Schlüter, H; König, S; Biel, K; Tepel, M; Zidek, W.

In: J VASC RES, Vol. 29, No. 3, 01.05.1992, p. 281-9.

Research output: SCORING: Contribution to journalSCORING: Journal articleResearchpeer-review

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Agha, A, Schlüter, H, König, S, Biel, K, Tepel, M & Zidek, W 1992, 'A novel platelet-derived renal vasoconstrictor agent in normotensives and essential hypertensives', J VASC RES, vol. 29, no. 3, pp. 281-9. https://doi.org/10.1159/000158943

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Bibtex

@article{58fa2c8472234b04b511ea6a121da704,
title = "A novel platelet-derived renal vasoconstrictor agent in normotensives and essential hypertensives",
abstract = "Platelet homogenates from 200 ml blood of essential hypertensives (n = 28) and normotensives (n = 13) were deproteinized and separated by gel chromatography. The fractions obtained were then tested for vasopressor activity in the isolated perfused rat kidney. In both normotensives and hypertensives, two vasopressor fractions appeared. There was no difference in vasopressor activity in the first vasoactive fraction between normotensives and hypertensives. In the second vasoactive fraction, the hypertensive patients showed a significant higher activity than the normotensive subjects (increase in perfusion pressure by 35.9 +/- 11.5 vs. 6.8 +/- 5.3 mmHg, p less than 0.01). This vasopressor fraction was not inhibited by saralasin, phentolamine, ketanserin, nitroprusside and daltroban and was effective after pretreatment with indomethacin and reserpine and in enzymatically deendothelialized kidneys. The effect was reduced by nifedipine and unchanged by heating the fraction at 100 degrees C and by incubation with proteinase K. It is concluded that a yet unidentified platelet-derived vasopressor agent may contribute to the enhanced vasoconstriction in essential hypertension.",
keywords = "Adenosine Triphosphate, Adult, Angiotensin II, Animals, Blood Platelets, Blood Pressure, Chromatography, Gel, Female, Humans, Hypertension, In Vitro Techniques, Male, Middle Aged, Norepinephrine, Rats, Rats, Inbred WKY, Reference Values, Renal Circulation, Serotonin, Sodium-Potassium-Exchanging ATPase, Tissue Extracts, Vasoconstrictor Agents, Journal Article, Research Support, Non-U.S. Gov't",
author = "A Agha and H Schl{\"u}ter and S K{\"o}nig and K Biel and M Tepel and W Zidek",
year = "1992",
month = may,
day = "1",
doi = "10.1159/000158943",
language = "English",
volume = "29",
pages = "281--9",
number = "3",

}

RIS

TY - JOUR

T1 - A novel platelet-derived renal vasoconstrictor agent in normotensives and essential hypertensives

AU - Agha, A

AU - Schlüter, H

AU - König, S

AU - Biel, K

AU - Tepel, M

AU - Zidek, W

PY - 1992/5/1

Y1 - 1992/5/1

N2 - Platelet homogenates from 200 ml blood of essential hypertensives (n = 28) and normotensives (n = 13) were deproteinized and separated by gel chromatography. The fractions obtained were then tested for vasopressor activity in the isolated perfused rat kidney. In both normotensives and hypertensives, two vasopressor fractions appeared. There was no difference in vasopressor activity in the first vasoactive fraction between normotensives and hypertensives. In the second vasoactive fraction, the hypertensive patients showed a significant higher activity than the normotensive subjects (increase in perfusion pressure by 35.9 +/- 11.5 vs. 6.8 +/- 5.3 mmHg, p less than 0.01). This vasopressor fraction was not inhibited by saralasin, phentolamine, ketanserin, nitroprusside and daltroban and was effective after pretreatment with indomethacin and reserpine and in enzymatically deendothelialized kidneys. The effect was reduced by nifedipine and unchanged by heating the fraction at 100 degrees C and by incubation with proteinase K. It is concluded that a yet unidentified platelet-derived vasopressor agent may contribute to the enhanced vasoconstriction in essential hypertension.

AB - Platelet homogenates from 200 ml blood of essential hypertensives (n = 28) and normotensives (n = 13) were deproteinized and separated by gel chromatography. The fractions obtained were then tested for vasopressor activity in the isolated perfused rat kidney. In both normotensives and hypertensives, two vasopressor fractions appeared. There was no difference in vasopressor activity in the first vasoactive fraction between normotensives and hypertensives. In the second vasoactive fraction, the hypertensive patients showed a significant higher activity than the normotensive subjects (increase in perfusion pressure by 35.9 +/- 11.5 vs. 6.8 +/- 5.3 mmHg, p less than 0.01). This vasopressor fraction was not inhibited by saralasin, phentolamine, ketanserin, nitroprusside and daltroban and was effective after pretreatment with indomethacin and reserpine and in enzymatically deendothelialized kidneys. The effect was reduced by nifedipine and unchanged by heating the fraction at 100 degrees C and by incubation with proteinase K. It is concluded that a yet unidentified platelet-derived vasopressor agent may contribute to the enhanced vasoconstriction in essential hypertension.

KW - Adenosine Triphosphate

KW - Adult

KW - Angiotensin II

KW - Animals

KW - Blood Platelets

KW - Blood Pressure

KW - Chromatography, Gel

KW - Female

KW - Humans

KW - Hypertension

KW - In Vitro Techniques

KW - Male

KW - Middle Aged

KW - Norepinephrine

KW - Rats

KW - Rats, Inbred WKY

KW - Reference Values

KW - Renal Circulation

KW - Serotonin

KW - Sodium-Potassium-Exchanging ATPase

KW - Tissue Extracts

KW - Vasoconstrictor Agents

KW - Journal Article

KW - Research Support, Non-U.S. Gov't

U2 - 10.1159/000158943

DO - 10.1159/000158943

M3 - SCORING: Journal article

C2 - 1324015

VL - 29

SP - 281

EP - 289

IS - 3

ER -