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Biomedical subjects

A F Sved

Publications and source records attributed to A F Sved.

At least 109 records · Page 6Linked to original sources
PubMed1986

Pontine pressor sites which release vasopressin.

Electrical stimulation of sites within the parabrachial nucleus (PBN; 0.2 ms pulses at 50 hz for 10 s, 100 microA) of chloralose-anesthetized rats elicited increases in mean arterial pressure (+ 34 +/- 2 mm Hg, n = 13). In rats in which the electrode tip was located in the dorsal and lateral portions of the PBN, electrical stimulation also produced a small increase in plasma levels of arginine vasopressin (VP; 6.7 +/- 0.9 pg/ml before stimulation to 16.5 +/- 3.9 pg/ml after, n = 7, P less than 0.05). No change in VP levels was observed with stimulation of more medial and ventral portions of the PBN. Following blockade of the autonomic nervous system (by i.v. injection of chlorisondamine plus infusion of phenylephrine to prevent hypotension) VP release in response to stimulation of the lateral and dorsal portions of the PBN was greatly enhanced (8.8 +/- 1.4 pg/ml following ganglionic blockade but before PBN stimulation and 82 +/- 27 pg/ml following stimulation, P less than 0.01) and this increase in VP release was sufficient to increase arterial pressure (+ 18 +/- 3 mm Hg, P less than 0.01). Electrical stimulation of the locus coeruleus (LC) produced a pressor response of similar magnitude to that produced by PBN stimulation. LC stimulation also increased plasma VP release (5.6 +/- 0.3 pg/ml before stimulation, 13 +/- 3 pg/ml following stimulation, and 30 +/- 8 pg/ml following stimulation in the ganglionic blocked state; n = 5).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Lack of change in high affinity glutamate uptake in nucleus tractus solitarius following removal of the nodose ganglion.

High affinity glutamate uptake in the intermediate portion of the nucleus tractus solitarius (NTS) was not altered by prior removal of one nodose ganglion or by prior midline transection at the level of the NTS. In contrast, glutamate uptake in a tissue punch of the septal nucleus was significantly reduced by prior transection of the fornix. Studies also compared septal glutamate uptake in crude homogenate, supernatant resulting from centrifugation at 3000 X g, and the pellet resulting from centrifugation at 17,000 X g. The results show quantitative differences between measures of glutamate uptake in these different fractions, but qualitatively the results were similar. (These results, do, however, suggest that glutamate uptake might be most appropriately measured in the pellet resulting from centrifugation at 17,000 X g.) The observation that removal of the nodose ganglion did not effect glutamate uptake in the NTS is therefore not due to the method by which glutamate uptake was assessed. These studies fail to replicate the previous observation that glutamate uptake in the NTS decreases following removal of the nodose ganglion, and thus question the hypothesis that glutamate is the neurotransmitter of vagal afferent fibers.

Animals↗
PubMed1986

Peripheral pressor systems in hypertension caused by nucleus tractus solitarius lesions.

The roles of vasopressin, the sympathoadrenal system, and the renin-angiotensin system in the production of hypertension after bilateral destruction of the nucleus tractus solitarius (NTS) were examined in chloralose-anesthetized rats. Since the activity of the renin-angiotensin system is high in anesthetized rats, additional studies were performed in unanesthetized, freely moving rats to evaluate the role of the renin-angiotensin system in hypertension caused by NTS lesions. Hypertension produced by bilateral electrolytic NTS lesions in rats was accompanied by elevated plasma levels of vasopressin (approximately 7-fold), norepinephrine (greater than 10-fold), and epinephrine (greater than 10-fold), but not of plasma renin activity. These results suggest that this form of hypertension is due to increased sympathoadrenal activity and increased vasopressin release into plasma and that the renin-angiotensin system is not involved. In rats with NTS lesions, blockade of vasopressin or the sympathoadrenal system, but not the renin-angiotensin system, elicited an acute decrease in arterial pressure. However, blockade of either vasopressin or the autonomic nervous system before production of the lesions had no effect on the resulting hypertension, indicating that in the absence of either one of these systems bilateral NTS lesions still result in severe hypertension. Although the renin-angiotensin system does not normally contribute to this hypertension, it does appear to contribute to the elevation in blood pressure once the actions of vasopressin have been blocked. In rats pretreated with a vasopressin antagonist, plasma renin activity increased following NTS lesions and the angiotensin converting enzyme inhibitor captopril decreased blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Medulla↗
PubMed1985

Elevated plasma vasopressin in cardiomyopathic hamsters.

Hamsters of the BIO 14.6 strain characteristically develop cardiomyopathy as they age, and hamsters of this strain have overt signs of heart failure by 11 months of age. Plasma levels of the posterior pituitary hormone arginine-vasopressin (AVP) were found to be elevated (approximately 2-fold) in 11 month old BIO 14.6 hamsters, compared to age-matched hamsters of a control strain. AVP appeared inappropriately elevated in these animals, since they were neither hyperosmotic nor markedly hypotensive. The elevated levels of AVP observed in these animals appears to contribute to vasomotor tone, since intravenous administration of a specific antagonist of the vasoconstrictor action of AVP [d(CH2)5Ome(TYR)AVP] elicited a fall in arterial pressure (9 +/- 2 mm Hg, n = 6, p less than 0.05). The AVP antagonist had no effect on arterial pressure in hamsters of a control strain, and vehicle administration had no effect on arterial pressure in either strain. These data indicate that inappropriately elevated levels of AVP contribute to the cardiovascular state of myopathic hamsters. Since elevated plasma AVP has been noted in human congestive heart failure, these results suggest that AVP may contribute to the cardiovascular status during congestive heart failure.

Age Factors↗
PubMed1985

Strain differences in pituitary prolactin content: relationship to number of hypothalamic dopamine neurons.

BALB/cJ mice have more tuberoinfundibular dopamine neurons, and thus greater tyrosine hydroxylase activity, than CBA/J mice. Strain differences in the synthesis and release of prolactin would also be predicted since dopamine released from the tuberoinfundibular neurons is the prolactin inhibitory factor which plays a role in the regulation of both prolactin synthesis and release. As expected, CBA/J mice, with fewer dopamine neurons, synthesized and released significantly more prolactin than BALB/cJ mice; that is, both pituitary and serum prolactin concentrations were greater in CBA/J mice. To determine if there were more cells containing prolactin or more prolactin per cell, pituitaries were stained with antibodies to prolactin and densitometric analysis made of both the average staining per unit area and total staining per pituitary. For both indices CBA/J mice had more staining than BALB/cJ mice. Using these criteria the difference in staining was attributed to more prolactin-stained lactotrophs in the CBA/J strain. Although no differences in the number of acidophils demonstrated by Pearse Trichrome method were observed, acidophils from BALB/cJ mice appeared smaller and contained less cytoplasm than those from CBA/J mice. We conclude that strain differences in the number of tuberoinfundibular dopamine neurons are inversely related to the number of immunocytochemically demonstrable prolactin-containing cells in the anterior pituitary.

Animals↗
PubMed1985

Cerebellar lesions attenuate vasopressin release in response to hemorrhage.

The effect of bilateral lesions of the fastigial nucleus of the cerebellum on the release of vasopressin in response to a hypovolemic-hypotensive stimulus was examined in unanesthetized rats. Electrolytic lesions of the rostromedial fastigial nucleus decreased plasma vasopressin levels and attenuated the release of vasopressin in response to hemorrhage. These results suggest that the fastigial nucleus is involved in the regulation of vasopressin release to baroreceptor information and support a role of the fastigial nucleus in the response to hemorrhage.

Animals↗
PubMed1985

Clonidine can lower blood pressure by inhibiting vasopressin release.

The effect of clonidine on vasopressin release was studied in chloralose anesthetized rats which were made hypertensive by bilateral electrolytic lesions of the nucleus tractus solitarii (NTS). NTS lesions elevated arterial pressure and plasma vasopressin levels, and both of these variable were returned toward baseline values by intravenous injection of clonidine (30 micrograms/kg). Furthermore, the ability of a vasopressin antagonist to lower arterial pressure in NTS hypertensive rats was markedly attenuated by clonidine treatment. In contrast, autonomic blockade (chlorisondamine, 2.5 mg/kg) in NTS lesioned rats did not reduce plasma vasopressin levels or the effect of the vasopressin antagonist on blood pressure. These data demonstrate that part of the antihypertensive effect of clonidine in NTS hypertensive rats is due to inhibition of vasopressin release into the circulation.

Animals↗
PubMed1985

Caudal ventrolateral medulla can alter vasopressin and arterial pressure.

The effects of specific treatments of the caudal ventrolateral medulla (CVLM) on vasopressin (AVP) release and arterial pressure (AP) were examined in urethane-anesthetized rabbits. Electrical stimulation of the CVLM for 5 minutes did not increase plasma AVP; it did however elicit an acute fall in arterial pressure. Similarly, stimulation of cells in the CVLM by microinjection of L-glutamate caused an acute decrease in AP but no change in plasma AVP. Muscimol injected into the CVLM increased AP but not AVP. On the other hand, bicuculline decreased AP and markedly increased plasma AVP, and the increase in AVP following bicuculline injection was not secondary to the fall in AP. These results demonstrate that the CVLM is involved in the regulation of AVP release. Furthermore, taken together with previous findings, these studies indicate that AVP and AP respond differently to treatments of the CVLM, suggesting that different cells in the CVLM are involved in the regulation of AVP release and AP.

Animals↗
PubMed1985

Release of antidiuretic hormone in quadriplegic subjects in response to head-up tilt.

Plasma antidiuretic hormone (ADH) levels during head-up tilt were measured in quadriplegic patients and normal healthy subjects. In normal subjects, neither rapid tilt (from horizontal to 70 degrees head-up in 20 seconds and remaining head-up for 5 minutes) nor gradual tilt (from horizontal to 70 degrees head-up over 15 minutes) significantly changed the plasma ADH level. In contrast, rapid tilt elevated plasma ADH levels approximately fourfold in quadriplegic subjects. A less dramatic elevation in plasma ADH levels followed gradual tilt in quadriplegic subjects. These data, along with the possibility that the pressor potency of ADH is enhanced in quadriplegic subjects, suggest that ADH is involved in the maintenance of blood pressure in quadriplegics in a head-up position.

Adult↗
PubMed1985

Contributions of arginine vasopressin and the sympathetic nervous system to fulminating hypertension after destruction of neurons of caudal ventrolateral medulla in the rat.

We sought to determine the role in control of arterial pressure (AP) of the caudal ventrolateral medulla (CVL), a region containing noradrenergic neurons of the A1 group. Electrical stimulation of the A1 area in anaesthetized rats elicits a fall of AP and heart rate at low, but not high, stimulus frequencies. Electrolytic lesions of the A1 area produce fulminating hypertension and a 13-fold increase in plasma arginine vasopressin (AVP). A1-hypertension is attenuated by treatment with an AVP antagonist and is also diminished in rats of the Brattleboro strain. After AVP blockade, the residual hypertension is abolished by treatment with ganglionic or alpha adrenergic blockers, but not by adrenalectomy. We conclude that the region of the CVL containing the A1 noradrenergic cells tonically inhibits the discharge of sympathetic nerve activity as well as the release of AVP from the pituitary.

Adrenal Glands↗
PubMed1984

Dopamine synthesis in inbred mouse strains which differ in numbers of dopamine neurons.

BALB/cJ and CBA/J mice have been shown to have different numbers of dopamine (DA) neurons in the central nervous system, with BALB/cJ mice having 20-50% more DA neurons in each dopaminergic cell group which is reflected in a difference in tyrosine hydroxylase activity in these cell groups. The present study compared the levels of DA and the rate of DA synthesis between these two inbred mouse strains. Three measures were used to reflect the rate of DA synthesis: the levels of DA metabolites (DOPAC and HVA) in the striatum, the rate of disappearance of DA following inhibition of tyrosine hydroxylase with alpha-methyl-P-tyrosine, and the rate of accumulation of DOPA following inhibition of aromatic amino acid decarboxylase with NSD-1015. Striatal DA levels were slightly higher in CBA/J mice than BALB/cJ mice. The rate of DA synthesis in the striatum, as estimated from the accumulation of DOPA following NSD-1015 injection or from the decline of DA levels following alpha-methyl-p-tyrosine injection, was from 30-50% greater in the BALB/cJ mice compared to the CBA/J mice. In striatum, DOPAC levels were higher, HVA levels lower, and DOPAC plus HVA levels equal in CBA/J mice compared to BALB/cJ mice. The results show that BALB/cJ mice, with more DA neurons than CBA mice, also synthesize more DA. In addition, the data suggest that DA levels do not necessarily reflect numbers of DA neurons, and that catecholamine metabolite levels are not a good measure for comparing catecholamine synthesis between inbred animal strains.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1984

Strain difference in fear between spontaneously hypertensive and normotensive rats is mediated by adrenal cortical hormones.

In the present study we sought to determine whether the strain difference in fear reactivity between spontaneously hypertensive rats (SHR) and strain-matched WKY controls might be related to adrenocortical function. SHR and WKY were subjected to adrenalectomy prior to classical fear conditioning. Adrenal cortical steroids were replaced in some animals. Adrenalectomy produced comparable effects on conditioned fear reactivity in SHR and WKY and steroid replacement reversed the effects of adrenalectomy in both strains. However, a larger dose was required to compensate for adrenalectomy in SHR. These date implicate functions related, directly or indirectly, to the adrenal cortex, in the maintenance of the strain difference in fear reactivity.

Adrenal Cortex Hormones↗
PubMed1984

In vivo release by vagal stimulation of L-[3H] glutamic acid in the nucleus tractus solitarius preloaded with L-[3H] glutamine.

In anesthetized and paralyzed rats, using a push-pull perfusion technique, we examined the effect of bilateral vagal stimulation on the release of L-[3H] glutamic acid (L- [3H] Glu) from the nucleus tractus solitarius (NTS), after preloading the tissue either with L-[3H] Glu or L-[3H] glutamine (L- [3H] Gln). Vagal stimulation sufficient to produce a maximum fall of arterial pressure (AP) evoked release of L- [3H] Glu from the NTS when the tissue was preloaded with either 3H-Glu or 3H-Gln, and of D-[3H] aspartic acid (D-[3H] Asp) when this stable Glu analogue was used to preloaded with either 3H-Glu or 3H-Gln, and of D-[3H] precursor L-Gln is a good marker of the releasable pool of L-Glu in vivo and are consistent with the hypothesis that L-[3H] Glu is a neurotransmitter in the NTS, mediating the vasodepressor response from cardiopulmonary mechanoreceptors.

Afferent Pathways↗
PubMed1984

Inhibitory influences from arterial baroreceptors on vasopressin release elicited by fastigial stimulation in rats.

Electrical stimulation of the fastigial nucleus in anesthetized, paralyzed, and artificially ventilated rats for 10 seconds (50 Hz) induced a stimulus-locked elevation of arterial pressure (the fastigial pressor response) and increased plasma vasopressin. Cervical spinal cord transection abolished the stimulus-locked fastigial pressor response and augmented the vasopressin response to a 10-fold increase (19 +/- 1 to 188 +/- 58 pg/ml, P less than 0.05; n = 8). Grading the pressor elevations occurring during the fastigial nucleus stimulus changed the amounts of vasopressin released in the same animal: acute adrenalectomy and chemosympathectomy by guanethidine reduced the magnitude of the fastigial pressor response and facilitated the vasopressin release to fastigial nucleus stimulation (intact: 52 +/- 11 pg/ml; after adrenalectomy and chemosympathectomy, 254 +/- 73 pg/ml, P less than 0.05, n = 6). Subsequent intravenous administration of a bolus of phenylephrine to increase mean arterial pressure during fastigial nucleus stimulus, as in intact situation, reduced the vasopressin release (47 +/- 9 pg/ml). After sinoaortic denervation plus vagotomy, the fastigial pressor response was preserved; however, vasopressin still increased 11-fold (from 11 +/- 1 to 126 +/- 23 pg/ml, P less than 0.01, n = 8). Vagotomy alone did not affect the vasopressin resting level nor the 4-fold increase in response to fastigial nucleus stimulation. Therefore, stimulus-locked elevations of arterial pressure oppose, by reflex mechanisms mediated through baroreceptors, but do not prevent the release of vasopressin elicited by stimulation of the fastigial nucleus.

Animals↗
PubMed1984

Arterial pressure and plasma vasopressin: regulation by neurons in the caudal ventrolateral medulla of the rabbit.

Experiments in the anesthetized rabbit have demonstrated that the caudal ventrolateral medulla oblongata contains tonically active vasodepressor neurons which are themselves inhibited by GABAergic and glycine-like inputs. Alteration of neuronal function in this region also elevates plasma vasopressin levels, contributing to, but not completely accounting for, the hypertension and pulmonary edema observed after destruction of neurons in the region.

Animals↗
PubMed1984

Fastigial nucleus stimulation and concurrent activation of cardiovascular receptors; differentiate effects on arterial pressure, heart rate and vasopressin release.

The integrated effects of stimulation of fastigial nucleus (FN) and of concurrent activation of baroreceptors on arterial pressure (AP), heart rate (HR) and vasopressin (VP) release in anaesthetized, paralysed, artificially ventilated rats were investigated. Stimulation of FN blocked the fall in AP and HR elicited by afferent vagal stimulation. It also abolished the atropine-sensitive bradycardia occurring at the peak of the stimulus-elicited pressor elevation in 6-hydroxydopamine treated rats. Sinoaortic denervation plus vagotomy left the cardiovascular responses to FN stimulus unmodified but facilitated FN elicited VP secretion. Vagotomy alone was ineffective. After high spinal cord transection more VP than in the intact condition was secreted after FN stimulation: simultaneous afferent vagal stimulation did not affect the facilitated VP release. Therefore FN stimulation can inhibit the reflex effects on AP and HR from baroreceptors, while the high-(but not the low-) pressure receptors can partly inhibit the VP release elicited by FN stimulation.

Animals↗
PubMed1984

Tonic vasomotor control by the rostral ventrolateral medulla: effect of electrical or chemical stimulation of the area containing C1 adrenaline neurons on arterial pressure, heart rate, and plasma catecholamines and vasopressin.

We have studied the responses to electrical and chemical stimulation of the ventrolateral medulla in the chloralose-anesthetized, paralyzed, artificially ventilated rat. Locations of most active pressor responses were compared to regions containing neurons labeled immunocytochemically for phenylethanolamine N-methyltransferase (PNMT), the enzyme catalyzing the synthesis of adrenaline. Elevations of arterial pressure (+81.6 +/- 2.5 mm Hg) and cardioacceleration (+73 +/- 13.6 bpm) were elicited with low current (5 times threshold of 9.5 +/- 1.1 microA) electrical stimulation in a region of rostral ventrolateral medullary reticular formation we have termed the nucleus reticularis rostroventrolateralis (RVL). Electrical stimulation of the RVL increased plasma catecholamines (16.8-fold for adrenaline, 5.3-fold for noradrenaline, and 1.9-fold for dopamine) and vasopressin (1.7-fold before spinal transection, 4.7-fold after). The location of the most active pressor region in the ventrolateral medulla corresponded closely with the location of C1 adrenaline-synthesizing (PNMT-containing) neurons. In addition, the location of the most active pressor region in the dorsomedial medulla corresponded with the location of a bundle of PNMT-containing axons. Unilateral injections into the RVL of the excitatory amino acid monosodium L-glutamate (50 pmol to 10 nmol), but not saline, caused transient dose-dependent and topographically specific elevations (maximum +71.6 +/- 4.9 mm Hg) of arterial blood pressure and tachycardia. Injections of the rigid structural analogue of glutamate, kainic acid, caused large, prolonged (at least 15 min) pressor responses and tachycardia. Unilateral injections of the inhibitory amino acid gamma-aminobutyric acid (GABA) into the RVL caused transient dose-dependent hypotension (maximum -40.8 +/- 6.6 mm Hg) and bradycardia, whereas the specific GABA antagonist bicuculline caused prolonged (10 to 20 min) elevations (+64.2 +/- 6.8 mm Hg) of arterial pressure and tachycardia. By contrast, injections of the glycine antagonist strychnine had no significant effect. Bilateral injections of the neurotoxin, tetrodotoxin, dropped arterial pressure to low levels (51.7 +/- 4.7) not changed by subsequent spinal cord transection at the first cervical segment (52.5 +/- 6.2). We propose the following. (1) Neurons within the RVL, most probably C1 adrenaline-synthesizing neurons, exert an excitatory influence on sympathetic vasomotor fibers, the adrenal medulla, and the posterior pituitary. (2) These neurons are tonically active and under tonic inhibitory control, in part via GABAergic mechanisms--perhaps via the nucleus of the solitary tract (NTS).(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenalectomy↗