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Biomedical subjects

A F Sved

Publications and source records attributed to A F Sved.

122 records · Page 7Linked to original sources
PubMed1983

Fastigial stimulation releases vasopressin in amounts that elevate arterial pressure.

Electrical stimulation of the cerebellar fastigial nucleus (FN) in anesthetized, paralyzed, and artificially ventilated rat with a 10-s stimulus train (50 Hz) resulted in a stimulus-locked elevation in arterial pressure (AP) and heart rate, the fastigial pressor response (FPR). Blockade of autonomic effectors by chemosympathectomy (produced by treatment with 6-hydroxydopamine) combined with adrenalectomy, or by spinal cord transection at C1, abolished the FPR but unmasked an elevation of AP with longer latency (10-12 s) and duration (2-4 min), termed the residual FPR. The residual FPR was 1) abolished by midbrain transection, 2) blocked by administration of a specific antagonist of the vasopressor response to arginine vasopressin (AVP) [1,d(CH2)5Tyr(Me)AVP], and 3) was absent in homozygous and attenuated in heterozygous rats of the Brattleboro strain. FN stimulation elevated AVP threefold (from 13 +/- 1 to 38 +/- 8 pg/ml, P less than 0.02; n = 6) in intact rats and sevenfold in rats with combined chemosympathectomy and adrenalectomy (from 14 +/- 1 to 96 +/- 11 pg/ml, P less than 0.001; n = 9). Stimulation of the cerebellar FN can release AVP. In the absence of sympathoadrenal effectors, the amount so released is enhanced and capable of elevating AP.

Animals↗
PubMed1982

Destruction of noradrenergic neurons in rabbit brainstem elevates plasma vasopressin, causing hypertension.

When A1 noradrenergic neurons in the caudal ventrolateral medulla of rabbits are destroyed electrolytically or by local injection of the neurotoxin kainic acid, the concentration of vasopressin in plasma increases, causing hypertension. The A1 neurons may tonically inhibit the activity of vasopressin-secreting neuroendocrine cells through a direct hypothalamic projection.

Adrenergic Fibers↗
PubMed1982

Studies on the antihypertensive action of L-tryptophan.

The administration of L-tryptophan to spontaneously hypertensive rats caused a dose-related decrease in blood pressure. Maximal reductions occurred 2 hr postinjection. This effect could be attenuated by 1) coadministration of valine, an amino acid that competes with tryptophan for brain uptake; 2) pretreatment with metergoline, a serotonin receptor antagonist; and 3) pretreatment with parachlorophenylalanine, which inactivates tryptophan hydroxylase. In contrast, the effect of tryptophan on blood pressure could be enhanced by pretreatment with fluoxetine, a drug which blocks serotonin reuptake into presynaptic terminals. Taken together, these results indicate that tryptophan injection lowers blood pressure by a mechanism involving increased tryptophan uptake into brain, followed by enhanced conversion of the amino acid to serotonin (not tryptamine) and, ultimately, increased release of serotonin by brain neurons. The data thus support the notion that serotonergic neurons in the rat brain function in circuits that lower blood pressure.

Amino Acids↗
PubMed1980

Dietary protein intake influences the antihypertensive potency of methyldopa in spontaneously hypertensive rats.

When spontaneously hypertensive rats consumed a single meal before receiving methyldopa (MD), the increase in brain MD levels and the blood pressure reduction varied inversely with the meal's protein content. MD injection elicited a greater reduction in blood pressure (and a larger rise in brain MD) in spontaneously hypertensive rats consuming a protein-free meal than in fasting animals; it induced a smaller fall in blood pressure (and a smaller increase in brain MD) in spontaneously hypertensive rats ingesting a protein-containing meal than in fasting animals. This effect may depend on the large neutral amino acids contained in protein. Ingestion of a food identical in amino acid content to 18% casein, but containing an amino acid mixture instead of protein, also blunted the MD-induced fall in blood pressure. However, consumption of a similar diet, lacking the large neutral amino acids (but not other amino acids), elicited an MD-induced blood pressure reduction similar to that caused by ingesting a protein-free diet. The combined effects of meal consumption and MD injection on brain MD and blood pressure correlated significantly with the serum ration of MD to the sum of the natural large neutral amino acids and not with serum MD alone. Similar effects were also noted with chronic dietary and MD treatments. Thus, dietary protein content can influence significantly the potency of a clinically important amino acid drug that acts within the brain.

Amino Acids↗
PubMed1979

Tyrosine administration reduces blood pressure and enhances brain norepinephrine release in spontaneously hypertensive rats.

Administration of L-tyrosine to normotensive or spontaneously hypertensive rats reduces blood pressure. The effect is maximal within 2 hr of injection. In spontaneously hypertensive rats, a dose of 50 mg/kg, intraperitoneally, reduces blood pressure by about 12 mm Hg (1 mm Hg = 1.33 x 10(2) pascals); a dose of 200 mg/kg produces the maximal effect, a reduction of about 40 mm Hg. Tryptophan injection (225 mg/kg) also lowers blood pressure in spontaneously hypertensive rats, but only by about half as much as an equivalent dose of tyrosine. Other amino acids tested (leucine, isoleucine, valine, alanine, arginine, and aspartate) do not affect blood pressure. Tyrosine injection appears to reduce blood pressure via an action within the central nervous system, since the effect can be blocked by co-administering other large neutral amino acids that reduce tyrosine's uptake into the brain. That tyrosine's antihypertensive action is mediated by an acceleration in norepinephrine or epinephrine release within the central nervous system is suggested by the concurrent increase that its injection produces in brain levels of methoxyhydroxyphenylethylglycol sulfate.

Amino Acids↗
PubMed1979

Reduction in blood pressure in normal and spontaneously hypertensive rats by lergotrile mesylate.

The acute administration of lergotrile mesylate to normal or spontaneously-hypertensive rats (SHR) causes a prompt reduction in blood pressure. In SHR, doses as small as 0.05 mg kg-1 are effective; maximal reductions in blood pressure are obtained at a dose of 0.25 mg kg-1. Lergotrile may be administered intraperitoneally or orally. Its efficacy as an antihypertensive agent in rats does not diminish significantly when administered twice daily for 7 days. Although lergotrile has been reported to be a dopamine agonist, the present data do not establish the mechanism by which the drug lowers blood pressure.

Animals↗
PubMedDate not supplied

Neuroanatomical specificity of the circuits controlling sympathetic outflow to different targets.

1. Despite the emerging framework that central neural pathways controlling the activity of the sympathetic nervous system are capable of producing highly selective responses, the specific neural pathways governing different sympathetic outflows are poorly understood. 2. Anatomical studies suggest that five brain areas, namely the rostral ventrolateral medulla, the rostral ventromedial medulla, the caudal raphe nuclei, the region containing the A5 noradrenergic neurons and the paraventricular hypothalamic nucleus, provide dominant supraspinal innervation of sympathetic preganglionic neurons. 3. The anatomical parcellation of different functions within and among these cell groups is uncertain. However, recent studies using transynaptic retrograde labelling of neural pathways connected to various sympathetic targets suggest that the circuits controlling these different targets may be partially distinct. Similarly, anatomical studies relying on stimulus-evoked expression of immediate early genes, such as c-fos, suggest that different sympathetic responses may be controlled by distinct, neural circuits. 4. Thus, although many similarities exist in the anatomical circuits innervating different sympathetic targets, possibly supporting the orchestration of global sympathetic responses, differences are also discernible.

Adipose Tissue, Brown↗
PubMedDate not supplied

Vasopressin contributes to hypertension caused by nucleus tractus solitarius lesions.

Lesions of the nucleus tractus solitarius (NTS) were studied to determine whether they elevate plasma vasopressin levels and, if so, whether these elevated levels of vasopressin contribute to the hypertension caused by NTS lesions. Bilateral electrolytic lesions of the NTS caused acute, severe hypertension in rats anesthetized with chloralose and in conscious, freely moving rats. After placement of the NTS lesions there was a greater than tenfold elevation in plasma vasopressin levels. Administration of an antagonist of the vasoconstrictor action of vasopressin markedly diminished the hypertension in both conscious and anesthetized rats. Following ganglionic blockade with chlorisondamine, NTS lesions still elicited hypertension, and the magnitude of the hypertension was not different from that observed in rats not treated with chlorisondamine. The hypertension produced by lesions of the NTS in ganglionic-blocked rats was completely abolished by administration of a vasopressin antagonist. These results indicate that (1) NTS lesions elevate plasma vasopressin levels and (2) elevated plasma vasopressin contributes to the hypertension produced by such lesions.

Animals↗