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Biomedical subjects

H G Güllner

Publications and source records attributed to H G Güllner.

At least 19 recordsLinked to original sources
PubMed1984

Defective leukocyte adenylate cyclase function in hypokalemia.

Patients with hypokalemia due to Bartter's syndrome show an increase in adrenergic nervous system function with significantly elevated plasma norepinephrine excretion. Prolonged exposure to neurotransmitters or hormones is known to lead to a down-regulation of target-cell responsiveness. We measured cyclic AMP generation by leukocytes in response to the beta-adrenergic agonist isoproterenol and to prostaglandin E1 (PGE1) in six patients with Bartter's syndrome. As compared to normal controls, the response of cyclic AMP production by leukocytes to stimulation by 1-isoproterenol or PGE1 was significantly decreased. These results indicate that in Bartter's syndrome and probably in other diseases involving hypokalemia isoproterenol- and PGE1-sensitive adenylate cyclase activities of leukocytes are reduced. Because the effect of PGE1 on adenylate cyclase is not mediated through the specific beta-adrenoceptor, it is possible that a defect in receptor-adenylate cyclase coupling or a more distal post-receptor defect is responsible for the reduction in cyclic AMP production.

Adenylyl Cyclases↗
PubMed1984

Correction of polyuria by activation of adenylate cyclase in Brattleboro rats.

The diterpene forskolin has been demonstrated to activate adenylate cyclase in many tissues, independently of receptors, guanyl nucleotides or the guanine nucleotide regulatory protein. Rats with hereditary hypothalamic diabetes insipidus (Brattleboro strain) have a defect in the synthesis of vasopressin. This absence of vasopressin is reflected by polyuria and a decrease in the urinary excretion of cyclic AMP, which mediates the action of vasopressin in the epithelial cells of the collecting ducts. Treatment of Brattleboro rats or of control Long-Evans rats with forskolin in doses as low as 7 micrograms/animal produced a significant decrease in urine volume. The reduction in urinary volume was associated with a significant increase in the cyclic AMP content of renal medullary tissue. Thus, systemic activation of adenylate cyclase can correct the pathophysiological consequences of the absence of vasopressin.

Adenylyl Cyclases↗
PubMed1984

Hylambatin, a structurally unique tachykinin: effects on insulin and glucagon secretion.

Hylambatin is the first example of a tachykinin which possesses a methionyl methionine residue at the C-terminus, rather than the C-terminal tripeptide -Gly-Leu-Met-NH2 which hitherto has been a characteristic feature of all members of the tachykinin family. The effect of hylambatin on the secretion of glucoregulatory hormones was examined in the rat. Hylambatin, injected intravenously in graded doses 10 and 30 min before blood collection, significantly increased both plasma glucose and plasma insulin, whereas the secretion of glucagon was not affected. This profile of action is different from that of kassinin or substance P. Should hylambatin, like other neuropeptides, be present in mammalian tissue, it may have a role in the regulation of carbohydrate metabolism.

Animals↗
PubMed1983

The role of the adrenergic nervous system in sodium and water excretion.

There is considerable evidence that the renal nerves contribute to the regulation of salt and water excretion by a direct effect on tubular reabsorption, independent of changes in renal hemodynamics. Whereas the effect of the adrenergic nervous system on sodium reabsorption appears to be established in anesthetised animals, it has been suggested that the basal activity of the renal sympathetic nerves in conscious dogs is too low to have a significant effect on sodium reabsorption by the proximal tubules. However, denervation natriuresis and diuresis has recently been demonstrated in conscious euvolemic and conscious volume expanded rats. The effects of renal nerve stimulation on the handling of sodium and water by the proximal tubule can be mimicked by infusion of the alpha-adrenergic agonist norepinephrine and prevented by infusion of an alpha-adrenergic antagonist. This confirms that it is mediated by alpha-receptors. The adrenergic nervous system may have an independent role in the control of sodium excretion or may be complementary to other systems such as the renin-angiotensin-aldosterone system.

Adrenergic Fibers↗
PubMed1983

Regulation of sodium and water excretion by catecholamines.

There is considerable evidence that the renal nerves contribute to the regulation of salt and water excretion by a direct effect on tubular reabsorption, independent of changes in renal hemodynamics. Whereas the effect of the adrenergic nervous system on sodium reabsorption appears to be established in anesthetized animals, it has been suggested that the basal activity of the renal sympathetic nerves in conscious dogs is too low to have a significant effect on sodium reabsorption by the proximal tubules. However, denervation natriuresis and diuresis have recently been demonstrated in conscious euvolemic and conscious volume-expanded rats. The effects of renal nerve stimulation on the handling of sodium and water by the proximal tubule can be mimicked by infusion of the alpha-adrenergic agonist norepinephrine and prevented by infusion of an alpha-adrenergic antagonist. This confirms that they are mediated by alpha-receptors. The adrenergic nervous system may have an independent role in the control of sodium excretion or may be complementary to other systems such as the renin-angiotensin-aldosterone system.

Absorption↗
PubMed1983

A sibship with hypokalemic alkalosis and renal proximal tubulopathy.

A new syndrome, characterized by hypokalemic alkalosis, hyperreninemia, aldosterone, high urinary prostaglandin E2 excretion, normal BP, and resistance of BP to angiotensin II is described in three of four siblings. Histologic examination of tissue obtained by biopsy from the kidneys showed an intense staining of the proximal tubular cells, as well as an extreme hypertrophy of the proximal tubular basement membranes, features that previously have not been observed. On electron microscopic examination, the characteristic changes of the tubular cells consisted of very dense cytoplasm, compact mitochondria, and pyknotic nuclei. In contrast to Bartter's syndrome, the juxtaglomerular apparatus were of normal appearance. Glomerular filtration rate and renal plasma flow were within normal limits. Fractional distal delivery of proximal tubular solute and fractional chloride reabsorption in the thick ascending limb of the loop of Henle were normal. The findings of a genetic linkage between the syndrome and the major histocompatibility system suggests that this familial tubulopathy is an inherited disorder.

Aldosterone↗
PubMed1983

The interactions of prostaglandins with the sympathetic nervous system--a review.

In most isolated tissues, prostaglandins, particularly of the E-series, inhibit stimulated norepinephrine release from prejunctional nerve endings and inhibit sympathetic neurotransmission. They may also modulate the response of target organs to the neurotransmitter. In some tissues PGE enhances the response to norepinephrine. It appears that the effect of PGE on norepinephrine release is mediated by restriction of calcium availability at the nerve ending, although this mechanism is incompletely understood. Prostaglandins other than PGE do not appear to play a major role in the modulation of norepinephrine release. In the intact organism, prostaglandins facilitate norepinephrine release. Inhibition of prostaglandin synthesis causes a decrease in norepinephrine release. It is not clear if the effects in vivo are mediated by a direct action of prostaglandins or through baroreceptor reflex mechanisms.

Adrenergic Fibers↗
PubMed1983

Endogenously synthesized prostaglandins stimulate sympathetic nervous system activity.

We examined the effect of an increase of endogenous prostaglandin production, induced by potassium depletion, on the urinary excretion of the norepinephrine metabolites metanephrine, normetanephrine and MHPG. Potassium deficiency caused a significant increase in all three metabolites. Treatment with indomethacin, 10 mg/day for 5 days, partially reversed the increase in the urinary excretion of norepinephrine metabolites. These findings suggest that in the intact organism prostaglandins stimulate, rather than inhibit norepinephrine release. Stimulation of prostaglandin synthesis may lead to an increase in sympathetic nervous system activity by a direct action or via a baroreceptor feedback mechanism.

Animals↗
PubMed1983

Renal thromboxane excretion in Brattleboro rats with hereditary hypothalamic diabetes insipidus. Effect of vasopressin treatment.

Rats with hereditary hypothalamic diabetes insipidus (Brattleboro strain) which are devoid of vasopressin, excrete significantly increased amounts of immunoreactive thromboxane B2 in urine. The increase was corrected by treatment with vasopressin. These results suggest that, in the intact organism, thromboxane synthesis may be under tonic inhibitory control by vasopressin although other renal mechanisms explaining the increase in thromboxane cannot be excluded. Our observations further support an involvement of prostaglandins and thromboxanes in the regulation of water metabolism.

Animals↗
PubMed1983

Gastrin releasing peptide: endocrine functions in the rat.

The effect of porcine gastrin releasing peptide (GRP), a heptacosapeptide with potent gastrin releasing activity which has recently been isolated from porcine non-antral gastric tissue, on pituitary function was investigated in the rat. Graded doses of synthetic porcine GRP were injected intravenously and the animals were killed at various intervals after injection. Prolactin, growth hormone, luteinizing hormone (LH), follicle-stimulating hormone (FSH) and thyroid-stimulating hormone (TSH) were measured in serum by specific radioimmunoassays. GRP had no significant effect on prolactin, growth hormone or FSH serum concentrations at any dose or sampling time studied. In contrast, the heptacosapeptide significantly stimulated LH release and suppressed TSH secretion with injection of low doses. There are striking structural and some functional similarities between GRP and bombesin, an amphibian skin tetradecapeptide which shows amino acid homology with the C-terminal region of GRP. This suggests that the endocrine effects of GRP may be mediated by its bombesin-like residue.

Animals↗