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Biomedical subjects

T Unger

Publications and source records attributed to T Unger.

At least 343 records · Page 19Linked to original sources
PubMed1983

Differential regulation of beta-endorphin in the anterior pituitary, intermediate lobe, hypothalamus and brain stem.

The influence of adrenalectomy (adx), betamethasone (BET) and 11-deoxycorticosterone (DOC) on beta-endorphin-like-immunoactivity (beta-END-LI) in plasma, anterior (AP) and neuro-intermediate lobe (N-IL) of pituitary, hypothalamus (HT) and brain stem (BS) was studied in rats. One day or three weeks after adx animals were injected i.m. for five consecutive days with 0.4mg/kg BET or 3.4mg/kg DOC. Six days after adx beta-END-LI was increased in BS and plasma after four weeks there was an elevation in plasma and AP. BET suppressed beta-END-LI in plasma of both sham-adx and adx animals six days after operation and in the N-IL after six days of adx. DOC led to an increase of beta-END-LI in HT after sham-adx and to a reduction in the N-IL after four weeks of adx. These observations demonstrate that beta-END-LI is regulated differently at its sites of synthesis in the AP, N-IL and HT.

Adrenalectomy↗
PubMed1983

Oxytocin unlike vasopressin is a stress hormone in the rat.

The functions of oxytocin in the female are thought to be confined to the processes of milk ejection and parturition. In this study the role of oxytocin in the body's response to stressful stimuli has been examined. Physical immobilization of rats and forced swimming caused large increases in the secretion of the hormone, whereas vasopressin levels remained unchanged. These findings classify oxytocin, in contrast to vasopressin, as a so-called 'stress hormone' and suggest its importance in processes other than those related to reproduction.

Animals↗
PubMed1983

The tissue renin-angiotensin systems: focus on brain angiotensin, adrenal gland and arterial wall.

The enzyme renin has long been considered an exclusively renal enzyme responsible for the generation of angiotensin in the plasma, and angiotensin was considered a peptide hormone with specific target organs. Since renin has been discovered to occur not only in the kidney but in addition in a large number of other tissues, e.g. the salivary gland, the uterus, the blood vessels, the adrenal gland and the brain, this concept had to be revised. The possibility of local generation of angiotensin in these target tissues, where it has marked biological effects casts a new light on angiotensin as a more ubiquitous tissue factor or even a neurohormone.

Adrenal Glands↗
PubMed1983

Central effects of converting enzyme inhibitors.

Evidence has accumulated that systemic administration of converting enzyme inhibitors (CEI) such as captopril, MK 421 or SA 446 not only produces an inhibition of the plasma renin angiotensin system (RAS), but also of the RAS in various target organs which are relevant for blood pressure (BP) regulation. A potential target organ is the brain, where a local CE inhibition could contribute to the BP lowering action of CEI. CE in the brain can be inhibited by intracerebroventricular (i.c.v.) injection of CEI as evidenced by an inhibition of the pressor and drinking responses to i.c.v. angiotensin I (ANG I) or renin and by potentiation of the pressor responses to i.c.v. bradykinin. Site of the inhibition is not only the cerebrospinal fluid but also periventricular brain tissue such as the hypothalamus. I.c.v. injection of captopril at doses which inhibit brain CE but do not leak into the peripheral blood were shown to lower BP in conscious stroke-prone spontaneously hypertensive rats (SHRSP), but not in normotensive Wistar Kyoto (WKY) controls. Acute peripheral administration of CEI can produce an inhibition of brain CE. This was shown by an attenuation of the drinking responses to i.c.v. ANG I and renin and by direct measurements of CE activity in brain tissue. Chronic oral treatment with CEI produces changes of brain RAS parameters which suggest an inhibition of ANG II formation in the brain.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1983

Pharmacology of converting enzyme inhibitors: new aspects.

The antihypertensive mechanism of CEI cannot be solely explained by an inhibition of the plasma RAS with reduced vasoconstrictor action of circulating ANG II. Inhibition of Kininase II with an increase of endogenous bradykinin does not appear to play a major role. Within the dose range used therapeutically, captopril and other CEI inhibit the facilitatory action of ANG II on neurogenic vasoconstriction, leading to a reduced sympathetic tone. CEI may also interfere with sympathetic reflexes. Doses above the therapeutic range seem to inhibit the sympathetic nervous system through mechanisms unrelated to CE inhibition. A reduced local generation of ANG II within tissues such as vascular wall, kidney or brain appears to contribute sympathetic tone. The type of hypertension (e.g. with or without stimulated plasma RAS or sympathetic tone) and the chemical characteristics of the CEI used (e.g. lipid solubility governing penetration into tissues) may determine the relative importance of the different mechanisms and sites of action for the reduction of blood pressure.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1983

The brain angiotensin system: subcellular localization and interferences with converting enzyme inhibitors.

Renin is stored in synaptosomes of rat brain, separately from cathepsin D and intraneuronal angiotensin II (ANG II) has been demonstrated with the electron-microscope. Although the subcellular localization of other components of the renin-angiotensin system (RAS) have still to be investigated, these data suggest possible intracellular synthesis of ANG II in the brain. Brain ANG II is biochemically identical to the plasma peptide and corresponds to (IIe) 5-ANG II. The peptide level is unchanged after bilateral nephrectomy, and angiotensin I (ANG I) accumulation is observed in nephrectomized animals following brain angiotensin converting enzyme blockade. The significantly greater accumulation of ANG I and reduction of ANG II in stroke prone spontaneously hypertensive Wistar-Kyoto rats (WKY) indicates a higher synthesis and turnover rate of ANG II in SHR. Most converting enzyme inhibitors (CEI) penetrate the brain after chronic oral treatment. Part of their blood pressure lowering action may therefore be explained by an inhibition of the brain RAS.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1982

Evidence against co-storage of enkephalins with noradrenaline in bovine adrenal medullary granules.

Bovine adrenal chromaffin granules were purified and separated into adrenaline (A) and noradrenaline (NA) containing granule populations by a combination of differential and isopycnic gradient centrifugation. The distribution of [Leu5]enkephalin as measured by radioimmunoassay followed a pattern identical to adrenaline but not noradrenaline on centrifugation. This suggests that enkephalins are stored in the same type of granule where adrenaline is found or that enkephalins and adrenaline even coexist in one and the same granule. Enkephalins may therefore function as co-transmitters or co-hormones of adrenaline rather than noradrenaline in the adrenal medulla.

Adrenal Medulla↗
PubMed1982

The intrarenal renin-angiotensin-system. An immunocytochemical study on the localization of renin, angiotensinogen, converting enzyme and the angiotensins in the kidney of mouse and rat.

The localization of renin, converting enzyme (CE) and angiotensin II (ANG II) in the kidneys of rats and mice was investigated with immunocytochemical methods. According to the presence and specific intrarenal localization of these components of the renin-angiotensin-system (RAS) our results suggest that in addition to the well known systemic effects of the RAS, there are interactions of its components inside the kidney. These interactions may lead to the generation of an extra portion of ANG II in the renal blood stream with its target cells determined by the localization of CE at the luminal side of well defined endothelial areas. These intrarenal-intravasal reactions may or may not reinforce the action of "systemic" ANG II, generated prerenally. In addition, the existence of true intrarenal-interstitial interactions, with the different components and actions of this intrarenal RAS restricted entirely to the kidney is suggested by our results, particularly the demonstration of ANG II within epitheloid cells and the dissociation of systemic renin and ANG II from their local concentrations in renal hypertensive rats.

Angiotensinogen↗
PubMed1982

Angiotensin stimulates oxytocin release: imparied response in rats with genetic hypothalamic diabetes insipidus.

Intracerebroventricularly (i.c.v.) administered angiotensin II (ANG II) at a dose of 100 ng caused a large increase in plasma oxytocin levels in Long Evans (LE) rats and in rats heterozygous for hypothalamic diabetes insipidus (HZ). In rats homozygous for diabetes insipidus (DI) even 100 fold higher doses of ANG II i.c.v. exerted only marginal effects on oxytocin release. The impaired responsiveness in DI rats was fully restored by prolonged treatment with a vasopressin (AVP) analogue. These data show that the decreased sensitivity of ANG II receptors in DI rats is due to the AVP defect and its metabolic consequences and can be reversed by AVP substitution.

Angiotensin II↗
PubMed1982

Distribution of neurophysins in rat brain: radioimmunological measurement and characterization.

Rat neurophysins were isolated from posterior pituitaries and antibodies raised in rabbits. Individual sensitive and specific radioimmunoassays for the neurophysins associated with either vasopressin or oxytocin were developed and employed for measuring the neurophysins in various regions of rat brain. Neurophysin-like immunoreactivity was detected in hypothalamus, septum, amygdala, brainstem and spinal cord. Characterization by high performance liquid chromatography suggested the identity with the neurophysins contained in the posterior pituitary. The distribution of these peptides in the brain points to a possible role in central nervous system processes.

Animals↗
PubMed1982

Dissociation between in vivo and in vitro measurements of converting enzyme activity after chronic oral treatment with captopril in rats.

Intravenous administration of captopril (20 micrograms) produced inhibition of angiontensin I pressor responses by 70 percent and of plasma-converting enzyme activity by 72 percent. Oral treatment with captopril (50 mg/kg/day) for 1 week inhibited angiotensin I pressor responses more (84 percent) than plasma-converting enzyme activity (23 percent). Four month oral treatment of normotensive and spontaneously hypertensive rats with captopril (50 mg/kg/day) led to 68 and 71 percent inhibition of angiotensin I pressor responses, but produced increases in plasma-converting enzyme activity of 123 and 94 percent, respectively. In spontaneously hypertensive rats, elevated converting enzyme activity in the medulla oblongata was measured after this treatment. It is concluded that plasma-converting enzyme activity measurements can be dissociated from the in vivo inhibition of converting enzyme. Chronic oral captopril treatment results in an induction of converting enzyme biosynthesis not only in peripheral tissue but also in the brain.

Angiotensin I↗
PubMed1982

SA446, a new orally active converting enzyme inhibitor: antihypertensive action and comparison with captopril in stroke-prone spontaneously hypersensitive rats.

The converting enzyme inhibitors (CEI) SA446 and Captopril (CAP) were given orally at a dose of 50 mg/kg per day to adult stroke-prone spontaneously hypertensive rats (SHRSP) over a period of four weeks. Both CEI lowered arterial blood pressure (BP) to a similar extent. CAP was more inhibitory on the plasma renin-angiotensin system (RAS) than SA446. Both CEI lowered urinary aldosterone excretion but had little (SA446) or no (CAP) natriuretic effect. CAP reduced the pressor responses to intravenous (i.v.) angiotensin I (ANG I) more (52%) than SA446 (18%) and potentiated the depressor responses to i.v. bradykinin more (fortyfold) than SA446 (tenfold). In contrast, SA446 treatment reduced the pressor responses to intracerebroventricular (i.c.v.) ANG I by 21% and led to a rise in the hypothalamic renin concentration. Oral CAP treatment for four weeks did not produce these signs of a brain converting enzyme inhibition. It is concluded that SA446 is equally as antihypertensive as CAP in SHRSP. SA446 appears to penetrate more readily into the brain and to exert its action partly through inhibition of the brain RAS which is known to be stimulated in SHRSP.

3-Mercaptopropionic Acid↗
PubMed1982

Amino acid-p-nitroanilide and -beta-naphthylamide cleaving activities in rat serum.

Determination of proteolytic activities gains increasing importance for the diagnosis of various pathologic conditions. Many questions can only be solved with the aid of experiments with animals. In preparation of such studies the pattern of the enzymatic hydrolysis of 20 amino acid-p-nitroanilides and one -beta-naphthylamide by normal rat serum was measured. The pH dependences of the single reactions are reported as well as their sensitivity to the action of ethylenediaminetetraacetic acid, dithioerithrol, and puromycin. Additionally, it is shown that collecting of the blood by cardiac puncture and preparation of the native plasma is the best way to get reproducible results.

Amino Acids↗
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↗