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Biomedical subjects

R E Lang

Publications and source records attributed to R E Lang.

At least 163 records · Page 9Linked to original sources
PubMed1983

Effects of lesions in the paraventricular nucleus of the hypothalamus on vasopressin and oxytocin contents in brainstem and spinal cord of rat.

The effects of lesions of the paraventricular nucleus in rat hypothalamus (PVN) on the vasopressin (AVP) and oxytocin (OT) contents of the brainstem and spinal cord, as measured by radioimmunoassay, were studied. AVP decreased by 50% and 80% in brainstem and spinal cord of lesioned animals, whereas OT disappeared almost completely. Therefore, in contrast to OT, the PVN is not the only site of origin of AVP-containing nerve fibers projecting to the brainstem.

Animals↗
PubMed1983

Evidence for the presence of enkephalins in the heart.

Extracts of guinea pig hearts were subjected to high performance liquid chromatography (HPLC) and the eluted fractions monitored by radioimmunoassays (RIA) for their content of leucine5-enkephalin (Leu-ENK) and methionine5 enkephalin (Met-ENK). Distinct peaks of both Leu-ENK and Met-ENK immunoreactivity were found corresponding to the position of synthetic Leu-ENK and Met-ENK respectively. The ratio of Leu-ENK to Met-ENK content was about 1:4. Chemical sympathectomy with 5-hydroxydopamine (6-OH-DA) produced a dramatic fall in noradrenaline content of the heart by more than 99%, whereas the concentration in Leu-ENK was reduced by only 70%. The Leu-ENK content of the adrenal glands was not affected by this treatment. These observations point to an enkephalinergic innervation of the heart which appears to be mainly of sympathetic origin. The results suggest the participation of enkephalins in cardiac reflex mechanisms.

Animals↗
PubMed1983

Effect of adrenalectomy and administration of hypertonic saline on the content of aldehyde fuchsin-positive neurosecretory material and posterior lobe hormones in the median eminence and the neural lobe of rats.

The influence of adrenalectomy and administration of hypertonic saline on the amount of vasopressin, oxytocin, and neurophysin contained in the median eminence and the neural lobe of rats was studied by means of the following methods: (i) morphometric and microphotometric analyses of aldehyde fuchsin-stained histological sections of the neurohypophysis; (ii) immunohistochemical demonstration of vasopressin, oxytocin, and neurophysin in the neurohypophysis, and (iii) radioimmunological measurement of vasopressin and oxytocin in extracts of the median eminence and the neural lobe. Adrenalectomy increases the amount of vasopressin and neurophysin in the external layer of the median eminence but does not change the content of oxytocin. It has no influence on the amount of vasopressin, oxytocin, and neurophysin demonstrable in the inner layer of the median eminence and in the neural lobe two weeks after the operation. Hypertonic saline markedly diminishes the vasopressin, oxytocin, and neurophysin content of the inner layer of the median eminence and the neural lobe but reduces only slightly, if at all, the amount of vasopressin and neurophysin in the outer layer of the median eminence. The findings support the concept that osmotic stress reduces only the vasopressin and oxytocin content of the hypothalamus-neural lobe system and has no or only little influence on the vasopressin content of the outer layer of the median eminence.

Adrenalectomy↗
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

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

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↗