PubMed Health⌕ Search

Biomedical subjects

D K Sundberg

Publications and source records attributed to D K Sundberg.

33 records · Page 2Linked to original sources
PubMed1981

Central neural peptides and catecholamines in spontaneous and DOCA/salt hypertension.

Hypothalamic and neurophypophyseal levels of catecholamines and peptides were measured in spontaneous and deoxycorticosterone (DOCA)/salt hypertension. Catecholamines, norepinephrine, epinephrine and dopamine were measured by electrochemical detection while the peptides, vasopressin, oxytocin, luteinizing hormone-releasing hormone (LHRH), the enkephalins and somatostatin (SRIF) were measured by radioimmunoassay. Blood pressure was significantly elevated in both groups as compared to their controls. Marked changes in central neural peptides were observed in the SHR, while no differences were seen in DOCA/salt hypertension. Hypothalamic vasopressin, oxytocin, LHRH and SRIF were significantly decreased. In the posterior pituitary, enkephalins were increased twofold in the SHR. With regard to catecholamines, there was no change in hypothalamic content. However, a dramatic decrease in neurohypophyseal dopamine was observed in SHR. Plasma levels of vasopressin were significantly elevated in both types of hypertension while oxytocin was increased only in the DOCA/salt model. These result show that (1) a wide spectrum of neuroendocrine changes are associated with genetic hypertension, (2) there are CNS differences between DOCA/salt and spontaneous hypertension, and (3) central aminergic changes may be involved in th neuroendocrine alterations seen in the SHR.

Animals↗
PubMed1981

Neurohypophyseal dopamine biosynthesis in the spontaneously hypertensive rat.

A study was performed to investigate the neurohypophyseal dopaminergic axis in terms of its biosynthetic activity and possible changes associated with spontaneous hypertension (SHR). An in vitro system was used in which isolated neuro-intermediate lobes were incubated with the catecholamine precursor, 3H-tyrosine. Dopamine (DA) content and 3H-DA were monitored using electrochemical detection coupled with high pressure liquid chromatographic separation. A time course study showed that there was significant incorporation of 3H-tyrosine into 3H-DA. In the SHR, both neurohypophyseal DA content and biosynthetic activity were reduced. Tissue levels of 3H-DA decreased from 651 to 297 dpm/posterior pituitary. A test of the effect of dehydration on neurohypophyseal dopaminergic activity revealed that water deprivation (48 hrs) caused an increase in DA biosynthesis in the hypertensive, but not the normotensive animal. This may have been due to a greater stimulation of the neurohypophyseal axis in the SHR since these animals showed significantly higher plasma vasopressin levels and hematocrits in response to dehydration. These results demonstrate that the neurohypophysis contains an active dopaminergic system which is altered in genetic hypertension.

Animals↗
PubMed1980

Hypothalamic catecholamine biosynthesis in vitro as measured by liquid chromatography and electrochemical detection.

A procedure is described for monitoring the biosynthesis of hypothalamic catecholamines in vitro, using the incorporation of the labeled precursor, 3H-tyrosine, into norepinephrine (NE), L-DOPAS and dopamine (DA). The technique involves separation of amines by high performance liquid chromatography, quantiation by electrochemical detection (LCEC), and the collection and measurement of labeled eluant. Rat hypothalami incubated in vitro were found to rapidly synthesize labeled DA while L-DOPA and NE synthesis were less apparent. The monoamine oxidase inhibitor, iproniazid, reduced incorporation. The tyrosine hydroxylase inhibitor, alpha methyl para-tyrosine (alpha mpt), virtually abolished DA synthesis while not appreciably affecting tissue content. The advantages of this technique over others is that it allows for the concurrent quantitation of tissue catecholamine levels, as well as their biosynthetic rate.

Animals↗
PubMed1976

The involvement of cyclic-3',5'-AMP in the release of hormones from the anterior pituitary in vitro.

DBcAMP significantly increased the release of GH but not of LH, FSH, TSH, or PRL, except in the presence of hypothalamic extract when it augmented the release of LH, FSH, and GH, reversed the inhibition of PRL, but did not further influence TSH release. Theophylline increased release of GH and PRL while inducing increased tissue content of cAMP without consistently increasing the release of TSH, LH, or FSH. Hypothalamic extractor K+-stimulated hormone rel-ase was consistently and significantly potentiated by theophylline. Neither hypothalamic extract, increased [K+], or synthetic TRH and LRH were able to raise tissue content of cAMP while producing their expected effects on hormone release. Cholera enterotoxin produced a highly significant increase in tissue content of the cyclic nucleotide but increased the release of GH only, and not that of LH, FSH, TSH, or PRL. DBcAMP was able to lower the threshold concentration of K+ required to stimulate release of GH, LH, and FSH and also to augment K+-stimulated release to the higher levels induced by the hypothalamic releasing hormones. It did not augment K+-induced release of TSH.

Adenosine Monophosphate↗
PubMed1975

Modification of brain and CSF LH-RH following deafferentation.

The effect of hypothalamic deafferentation upon levels of LH-RH in brain, cerebrospinal fluid, and plasma was studied in adult male rats. Deafferentation produced a significant increase in the LH-RH concentration of third ventricular CSF (from 140.6 to 343.9 pg/microl), while there was no change in median eminence or hypothalamic content. LH-RH in the pineal gland and the posterior pituitary was also elevated by hypothalamic isolation.

Animals↗
PubMed1975

The effect of various prostaglandins and a prostaglandin synthetase inhibitor on rat anterior pituitary cyclic AMP levels and hormone release in vitro (38475).

(U)Prostaglandins E-1, E2,F-1alpha or F-2 alpha significantly increased the release of GH, with a parallel increase in intracellular cAMP concentrations, while they only protentiated HE-stimulated TSH release. (2) None of the prostaglandins examined consistently effected either the basal or HE-altered release of LH,FSH or prolactin. (3) The prostaglandin synthetase inhibitor, indomethacin, inhibited GH and TSH release and, at high doses of the drug, inhibited prolactin release. In contrast, the drug appeared to potentiate both He and sLRF-stimulated gonadotropin release. It had no significant effect on intracellular cAMP concentration.

Animals↗
PubMedDate not supplied

Characterization of opioid peptides from maternal and fetal sheep adrenal glands.

Enkephalin immunoreactive material from adrenal glands was characterized both in maternal and fetal sheep at various gestational ages. Whole gland extracts from both maternal and fetal sheep contained three major peaks of Enk immunoreactivity corresponding to apparent molecular weights of 10,000, 2800, and less than 1200 daltons. The majority of maternal adrenal Enk immunoreactivity was found in medullary tissue, although cortex also contained low but detectable amounts. This was also the case in newborn lambs and 139 day fetuses, where adrenal cortex was sufficiently developed to allow extraction and quantitation of opioid material. In fetuses at mid-gestation (70-80 days), adrenal medullary Enk immunoreactivity was approximately 75% of maternal values. Met-Enk and Leu-Enk content in 139 day fetal medulla were 70 and 76% of maternal values respectively, while newborn Met- and Leu-Enk medullary content were similar to maternal values. The molar ratio of Met-Enk to Leu-Enk was approximately 4:1 in both maternal and fetal adrenal medulla, and 2:1 in adrenal cortex, suggesting different synthetic processing of opioid peptides in the two tissues. The early appearance of significant levels of adrenal medullary Enk immunoreactivity and subsequent development paralleling that of catecholamines suggest a predominant role for adrenal enkephalins in regulation of fetal cardiovascular function early in gestation.

Adrenal Cortex↗
PubMedDate not supplied

Catecholamine biosynthesis and vasopressin and oxytocin secretion in the spontaneously hypertensive rat: an in vitro study of localized brain regions.

The in vitro synthesis of catecholamines and the secretion of vasopressin (AVP) and oxytocin (OT) was measured in localized regions of the hypothalamo-neurohypophyseal system in the spontaneously hypertensive rat (SHR). The posterior pituitary (PP), median eminence (ME) and supraoptic (SON) and paraventricular (PVN) nuclear regions were incubated in vitro in media containing 3H-tyrosine. Media and tissue levels of AVP and OT were measured as well as norepinephrine and dopamine content and biosynthesis. There were no differences in peptide release in either the PP, ME or SON. However, there was a marked increase in peptide release from the PVN of the SHR. Media AVP levels were 0.3 pg/ml/micrograms protein in the WKY as compared to 2.1 pg/ml/micrograms protein in the SHR. OT release was increased 2 fold, from 0.85 to 1.7 pg/ml/micrograms protein. PVN content of both AVP and OT was significantly lower in the SHR. ME and SON peptide levels were not changed, while neurohypophyseal AVP levels were increased in the SHR. With regard to the catecholamines appreciable norepinephrine synthesis was measured in the PVN and SON while there was little 3H-norepinephrine in the ME or PP. In the hypertensive rat, there was an increase in norepinephrine synthesis in the PVN with no change in the SON. These results provide further support for fundamental changes in the catecholaminergic and peptidergic systems of the hypothalamo-neurohypophyseal axis of the SHR.

Animals↗
PubMedDate not supplied

Changes in paraventricular vasopressin and oxytocin during the development of spontaneous hypertension.

The potential role of central neuroendocrine changes in the development of spontaneous hypertension was evaluated. The developmental changes in blood pressure and hypothalamic and plasma levels of vasopressin (AVP) and oxytocin (OT) were determined in groups of SHR and WKY animals from 3 to 24 weeks of age. Hypothalamic OT content was significantly lower in 3-, 6-, and 12-week-old SHR rats compared to age-matched WKY animals. Hypothalamic AVP content was not different at 3 weeks of age, but was lower in the SHRs at 6 and 12 weeks. To localize strain differences in AVP and OT, specific hypothalamic nuclei were removed from 300 microns frozen brain sections, and hormone content measured. Paraventricular AVP and OT content was lower in the SHRs which had increased blood pressure (6, 12, and 24 weeks of age) but not in the prehypertensive groups (3 weeks of age). Neuropeptide content was unchanged in the supraoptic nucleus or median eminence. Plasma levels of AVP were increased in the SHR, while OT was unchanged. Thus, genetic hypertension is associated with specific and localized changes in hypothalamic AVP and OT. The fact that the peptide deficit occurred in the paraventricular nucleus, a region thought to be involved in the control of autonomic function, may have important implications in terms of the pathogenesis of hypertension.

Animals↗