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Biomedical subjects

D Ganten

Publications and source records attributed to D Ganten.

At least 433 records · Page 24Linked to original sources
PubMed1982

Renal kallikrein activity and urinary kallikrein excretion in rats with experimental renal hypertension.

1. Rats were made hypertensive by ligating the aorta between the origins of both renal arteries. Sham-operated animals served as controls. Urinary and renal kallikrein activities, as well as plasma and renal renin activities, were measured 8 and 90 days after surgery. 2. Blood pressure was 155 +/- 6 mmHg on day 8 after aortic ligature and 142 +/- 6 mmHg on day 90; in controls pressures were 107 +/- 3 and 110 +/- 5 mmHg respectively. 3. Eight days after aortic ligature, kallikrein activity in the ischaemic kidneys was about 6.5 times, and in the non-ischaemic kidneys almost 2 times, that in controls. After 90 days the kallikrein activity was reduced to one-half of that in the controls in the ischaemic kidneys and it was normal in the contralateral. 4. The urinary kallikrein excretion of hypertensive rats was about one-third of that of the controls at both 8 and 90 days after aortic ligature. 5. The plasma renin activity in hypertensive rats was approximately seven times that in control animal 8 days after aortic ligature and did not differ from the control value after 90 days. Renin activity in the kidneys showed the same pattern as in other models of renovascular hypertension: elevation in the ischaemic kidney and reduction in the non-ischaemic one.

Animals↗
PubMed1982

Vasopressin in brain of spontaneously hypertensive rats.

In stroke-prone spontaneously hypertensive rats (SHRSP) and in normotensive Wistar-Kyoto rats (WKY), arginine vasopressin (AVP) was measured by means of a radioimmunoassay in the plasma, the pituitary gland, the hypothalamus, and the brain stem. In 6- and 14-wk-old SHRSP, the plasma concentration of AVP was lower than in age-matched WKY (P less than 0.01), whereas it was elevated at 28 wk of age (P less than 0.01). In the pituitary of 6-wk-old SHRSP, AVP was higher than in WKY (P less than 0.05), but no such difference was found in older rats. In the hypothalamus and the brain stem, AVP content was reduced in all age groups of SHRSP. Plasma osmolality was diminished in 28-wk-old SHRSP only (P less than 0.01), whereas hematocrit in all age groups was higher in SHRSP than in WKY. It is concluded that the secretion of AVP and possibly its synthesis in the hypothalamus are reduced in SHRSP. Whether the reduced AVP content in the brain stem is related to the sustained elevation of blood pressure has to be studied further.

Aging↗
PubMed1982

Opioid peptides and blood pressure regulation.

Immunohistochemical and functional studies suggest that opioid peptides are involved in blood pressure regulation. Endorphin and enkephalins contained in the brain seem to exert their effects by mediation of cardiovascular centers in the brain stem. Additional effects on blood pressure may be exhibited by circulating opioid peptides released from the pituitary and adrenal gland which may act at both central and peripheral sites. It is expected that further studies will complete our knowledge about the interaction of opioid peptides and blood pressure regulation and will result in therapeutic applications.

Animals↗
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

Thirst in the rat after ligation of the inferior vena cava: role of angiotensin II.

The role of angiotensin II in thirst states after ligation of the inferior vena cava above (CLA) or below (CLB) the origin of the renal veins as compared to sham operated controls was evaluated 24 hrs after ligation. Water intake was enhanced in CLB rats and even more so in CLA rats. Plasma angiotensin II and urea concentrations and serum osmolality were increased in CLA rats. Plasma sodium concentration and hematocrit were reduced in CLA rats, and hematocrit in CLB rats as well. Water intake in CLA rats was retarded by IV infusions of saralasin. Saralasin infusions in CLA rats resulted in a dramatic increase of plasma angiotensin II concentrations. Ligation of the inferior vena cava induces major changes in body fluid homeostasis, which are more pronounced in CLA than in CLB rats. The increase in water intake in CLA rats appears to be partly mediated by angiotensin II.

Angiotensin II↗