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T Unger

Publications and source records attributed to T Unger.

At least 361 records · Page 20Linked to original sources
PubMed1981

[Pathophysiology of essential hypertension. Recent findings (author's transl)].

The blood pressure is regulated by the relationship of cardiac output and peripheral resistance to each other. Both parameters are influenced by the heart, by the kidneys and by the resistance vessels. For a long time the main objective of hypertension research has been directed towards these end organs of circulatory regulation. The functional condition of the heart, kidneys and arterioles is, however, decisively controlled and integrated by the brain. The newly discovered neuropeptides of recent years seem to fulfil an important function in the central mechanisms of circulation regulation. The autonomic nervous system and the hypothalamic and hypophyseal hormones have been discussed as peripheral mediators of the cardiovascular control centers in the brain.

Angiotensin II↗
PubMed1981

In vivo activity of purified mouse brain renin.

Mouse brain renin and kidney renin were purified by a 3-step procedure: acetone powder extraction. Sephadex G-100 chromatography, and blue agarose affinity chromatography. The latter efficiently separated from cathepsin D-like acid protease activity. Mouse brain renin had an optimum of enzyme activity of pH 7.0. This differed from mouse kidney renin, which had an optimum at pH 8.5. In vitro, brain renin formed angiotensin I from rat plasma angiotensinogen and had no angiotensinase activity. Mouse brain renin was inhibited by monospecific antibodies raised against pure mouse submandibular gland renin. In vivo activity of the enzyme was tested by injection of brain renin into the lateral brain ventricle of rats. This resulted in the formation of angiotensin I from endogenous brain angiotensinogen, in the stimulation of water uptake, and in a long-lasting increase of arterial blood pressure. The latter could be blocked by the competitive angiotensin II receptor antagonist, saralasin. The results showed that brain renin is active under physiological conditions.

Angiotensin II↗
PubMed1981

Plasma-converting enzyme activity does not reflect effectiveness of oral treatment with captopril.

Intravenous Captopril (20 microgram) in rats produced similar inhibition of the pressor responses to intravenous ANG I (70%) and of plasma-converting enzyme activity (CEA) measured fluorometrically (72%). One week oral treatment with Captopril (50 mg/kg per day) inhibited ANG I pressor responses more (84%) than plasma CEA (23%). Four-month oral treatment of normotensive and spontaneously hypertensive rats with Captopril (50 mg/kg per day) led to a 68% and 71% inhibition of the ANG I pressor responses, but to a 123% and 94% increase of plasma CEA, respectively. Thus, plasma CEA measurements can be dissociated from the in vivo inhibition of converting enzyme (CE). Chronic oral Captopril treatment induces CE biosynthesis.

Angiotensin I↗
PubMed1981

Reduced content of vasopressin in the brain of spontaneously hypertensive as compared to normotensive rats.

Arginine-vasopressin (AVP) content was measured by radioimmunoassay in the plasma and brain of stroke-prone spontaneously hypertensive rats (SHRsp) and normotensive Wistar Kyoto (WKY) control rats. AVP was reduced in plasma, hypothalamus, amygdala, septum and brain stem of the hypertensive animals. In view of the possible sensitizing effect of vasopressin on the baroreceptor reflex, the reduction of this peptide in the brain stem could contribute to hypertension in SHRsp.

Animals↗
PubMed1981

Central blood pressure effects of substance P and angiotensin II: role of the sympathetic nervous system and vasopressin.

The role of the sympathetic nervous system and of arginine vasopressin (AVP) in the mediation of the central cardiovascular effects of angiotensin II (ANG II) and substance P (SP) was investigated. ANG II and SP caused dose-dependent blood pressure increases when injected into the lateral brain ventricle (i.c.v.) of conscious rats; ANG II was tenfold more potent than SP. Peripheral blockade of alpha-adrenoceptors with prazosin or blockade of the vasopressor action of AVP by the AVP antagonist d(CH2)5VDAVP both partially inhibited the pressor responses to central ANG II. Combined treatment with the two blockers produced almost complete inhibition of the central ANG I responses. Substance P injected i.c.v. produced increases in noradrenaline and adrenaline but not AVP in the plasma. Peripheral alpha-receptor blockade by prazosin reversed the central pressor effects of SP to depressor responses. The AVP antagonist did not alter the cardiovascular responses to SP. It is concluded that in conscious animals, stimulation of the sympathetic nervous system and release of AVP contribute to the central pressor action of ANG II to a similar extent and independently of each other. In contrast, the central pressor responses to SP appear to be exclusively mediated by the sympathetic nervous system without participation of AVP.

Angiotensin II↗
PubMed1981

Brain converting enzyme inhibition: a possible mechanism for the antihypertensive action of captopril in spontaneously hypertensive rats.

The effects of various doses of the converting enzyme inhibitor captopril injected into the lateral brain ventricle (i.c.v.) and intravenously (i.v.) on blood pressure (BP) and on converting enzyme activity were tested in stroke prone conscious spontaneously hypertensive rats (SHR-sp) and in normotensive Wistar Kyoto rats (WKY). Injection of 500 micrograms captopril i.c.v. produced a marked biphasic BP effect in SHR-sp, an initial increase followed by a long-lasting decrease. Only the initial BP increase was observed in WKY. The pressor responses to i.c.v. angiotensin I (ANG I) were completely blocked after i.c.v. captopril injection and this effect lasted for 24 h. The pressor responses to i.v. ANG I were also inhibited immediately after 500 micrograms captopril i.c.v. and gradually returned to control values within 5 h. Intravenous injections of 500 micrograms captopril almost completely inhibited the pressor responses to i.v. ANG I; they caused a moderate BP decrease in SHR-sp and had no significant BP effects in WKY. In SHR-sp, 5 micrograms captopril i.c.v. caused a reduction of BP with a concomitant inhibition of the pressor effects of i.c.v. ANG I. Both effects lasted about 30 min. The pressor responses to i.v. ANG I were not inhibited. In WKY, 5 micrograms captopril i.c.v. had no effect on BP. It is concluded that captopril can reduce BP by action on the brain without peripheral inhibition of converting enzymes. Following high doses injected i.c.v., the inhibitor leaks into the periphery but this cannot explain the marked hypotensive effect in SHR-sp.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1981

Converting-enzyme in the choroid plexus, brain, and kidney: immunocytochemical and biochemical studies in rats.

In rats, immunoreactivity was demonstrated in the brush border of the choroid plexus, in the wall of blood vessels in the brain, and in the brush border of the proximal tubules of the kidney, using the peroxidase-antiperoxidase technique (PAP) and an anti-pulmonary converting-enzyme antibody. These findings correlate with biochemical data of converting-enzyme activity in the choroid plexus and in other tissues. Possible functions of the enzyme in relation to its localization are discussed.

Animals↗
PubMed1981

Acute sino-aortic denervation in rats produces a selective increase of adrenaline turnover in the dorsal midline area of the caudal medulla oblongata and a reduction of adrenaline levels in the anterior and posterior hypothalamus.

Acute sino-aortic denervation produces an acute reduction of adrenaline stores in the anterior and posterior hypothalamus and a reduction of noradrenaline stores in the dorsal midline area of the caudal medulla oblongata. Furthermore, removal of baroreflex afferents results in an increase of adrenaline turnover in the DCMO but not in the hypothalamus. The present findings give evidence for participation of adrenergic mechanisms in central baroreflex regulation. The findings can be interpreted according to the adrenaline vasodepressor hypothesis of hypertension.

Animals↗
PubMed1981

Equipotentiality of function in dichotic listening.

Listeners who had demonstrated right-ear dichotic listening preference in the first of four listening sessions were randomly assigned to an experimental and control group. Both groups participated in three more dichotic listening sessions. For sessions 2 and 3, left-ear responses were reinforced for the experimental group listeners. There was a significant interaction between groups and sessions. After a drop to equal numbers of right- and left-ear responses in session 2, the control group demonstrated significant right-ear preference in sessions 3 and 4. The responses of the experimental group showed strong left-ear preferences in sessions 2 and 3. Their left-ear gains were preserved in session 4, while their right-ear responses returned to the level demonstrated in session 1. It was concluded that the experimental group had learned to attend to and report left-ear stimuli without loss of right-ear report competence. Within the experimental paradigm, equipotentiality of function has been demonstrated.

Adult↗
PubMed1981

Vasopressin-induced increase in total peripheral resistance in deoxycorticosterone acetate hypertensive rats is buffered by the baroreceptor reflex.

1. The role of arginine-vasopressin (AVP) in the maintenance of high blood pressure in rats with deoxycorticosterone acetate (DOCA) hypertension was investigated. 2. Plasma concentrations of AVP were significantly elevated in DOCa hypertensive rats compared with normotensive control rats, whether or not they received 1% sodium chloride solution or demineralized water to drink. 3. The specific antagonist of the vasopressor response to AVP, d(CH2)5VDAVP (100 microgram/kg intravenously), significantly increased cardiac output and decreased total peripheral resistance, but had no effect on mean arterial pressure in DOCA hypertensive rats. No changes of mean arterial pressure, cardiac output and total peripheral resistance were observed in the normotensive control groups after d(CH2)5VDAVP. 4. After sino-aortic baroreceptor deafferentation, d(CH2)5VDAVP decreased mean arterial pressure in DOCA--salt hypertensive rats, but not in the control groups. 5. It is concluded that elevated circulating AVP causes vasoconstriction in DOCA hypertensive rats. The AVP-induced increase in total peripheral resistance is counter-regulated by an activation of the baroreceptor reflex and subsequent reduction in cardiac output.

Animals↗
PubMed1980

Blood pressure and heart rate responses to centrally administered substance P are increased in spontaneously hypertensive rats.

1. The cardiovascular effects after intracerebroventricular injections of substance P were investigated in normotensive Wistar-Kyoto and in spontaneously hypertensive rats. 2. Substance P increased blood pressor in both rat strains. Wistar-Kyoto rats responded with moderate, dose-dependent blood pressure increases, and heart rate decreased; spontaneously hypertensive rats showed two- to three-fold increased pressor effects and, concomitantly, marked heart rate increases to intracerebroventricular injections of substance P. 3. Sino-aortic baroreceptor denervation rendered Wistar-Kyoto rats supersensitive to intracerebroventricular substance P to a similar degree as unoperated spontaneously hypertensive rats. Sino-aortic denervation had no effect on the blood pressure responses to the peptide in spontaneously hypertensive rats. 4. The central pressure actions of substance P could be markedly attenuated by intracerebroventricular pretreatment with the derivative of gamma-aminobutyric acid, baclofen. 5. We conclude that the baroreceptor reflex is disturbed in spontaneously hypertensive rats. Substance P may contribute to the pathogenesis of hypertension. The effector pathways appear to be different from angiotensin.

Angiotensin II↗
PubMed1980

Is arterial media hypertrophy in spontaneously hypertensive rats a consequence of or a cause for hypertension?

1. The increased peripheral resistance observed in established hypertension has been attributed to structural changes in the resistance vessels, which are considered to be due mainly to medial hypertrophy. This study was undertaken to examine the possibility that structural changes in the arterial bed are genetically determined and may be causative factors in the development of high blood pressure in the spontaneously hypertensive rat. 2. The wall dimensions of aorta, renal artery and intrarenal arteries down to a distended diameter of 35 micrometer were studied: (a) in 14-week-old spontaneously hypertensive rats; (b) in age- and sex-matched spontaneously hypertensive rats which had been treated with captopril for two generations and had been normotensive during their complete life span; (c) in normotensive Wistar-Kyoto control rats. 3. Cross-sectional areas of the media were increased in the hypertensive rats in comparison with 'normotensive spontaneously hypertensive rats' and Wistar-Kyoto rats. Increased numbers of smooth muscle cells were found in the major arteries of hypertensive animals. 4. These results indicate that hypertrophy of the media is a consequence of high blood pressure rather than a genetically determined pathogenetic factor for the development of hypertension in spontaneously hypertensive rats.

Animals↗