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J M Sitsen

Publications and source records attributed to J M Sitsen.

22 records · Page 2Linked to original sources
PubMed1981

Beta-Endorphin, an endogenous depressor agent in the rat?

1. The role of opiates in cardiovascular regulation has been investigated. 2. In urethane-anaesthetized renal hypertensive rats (two-kidney, one-clip Goldblatt model), intracerebroventricular beta-endorphin (10 microgram) caused a greater fall in mean arterial pressure than in sham-operated controls. 3. Unilateral injection of beta-endorphin into the nucleus tractus solitarii of the urethane-anaesthetized rat resulted in a U-shaped dose--response relationship, with a fall in mean arterial pressure and heart rate occurring at low doses. Doses above 10 ng caused a rise in pressure, accompanied by a variable effect on heart rate. 4. The fall in blood pressure and heart rate was prevented by prior subcutaneous administration of naloxone. Naloxone caused an increase in blood pressure when administered alone. 5. These results suggest a depressor role of an endogenous brain opiate, possibly beta endorphin; a site of action is probably the nucleus tractus solitarii.

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Hypoalgesia in genetically hypertensive rats (SHR) is absent in rats with experimental hypertension.

In this study a possible relationship between regulatory mechanisms involved in pain and blood pressure control has been investigated in the rat. Spontaneously hypertensive rats (SHR), their normotensive Wistar-Kyoto (WKY) controls, and two experimental models of hypertension together with their appropriate sham-operated controls were tested for their responsiveness to pain. Two methods for measurement of nociceptive responsiveness (hot plate and electric footshock threshold) were used. A diminished responsiveness was observed in both young (still normotensive) and adult (hypertensive) SHR. Pretreatment with naloxone reduced hot plate response times of adult SHR to the level of WKY, indicating opioid receptor involvement. Despite severe hypertension in rats with a renal artery clip and in DOCA-salt treated rats, no reduction of pain sensitivity as compared to sham-operated controls was evident in the hypertensive rats as assessed by both methods. It is concluded, that the higher pain threshold in SHR is probably determined by genetic factors rather than hypertension.

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PubMedDate not supplied

Cardiovascular and respiratory effects of beta-endorphin in anesthetized and conscious rats.

This study deals with the effects of beta-endorphin on blood pressure, heart rate, and respiratory frequency in anesthetized and conscious rats after both peripheral and central administration. Intravenous injection of beta-endorphin (40 and 160 micrograms/kg) in urethane-anesthetized rats resulted in a prolonged decrease in blood pressure, which, after the higher dose, was accompanied by bradycardia. In the pentobarbitone-anesthetized animals the same doses of beta-endorphin caused a small rise in blood pressure without affecting heart rate. No effect on respiratory frequency was observed. In urethane-anesthetized rats with hemorrhagic shock intravenous naloxone elicited a small pressor effect. Intracerebroventricular injection (i.c.v.) of beta-endorphin (40 micrograms/rat) in urethane-anesthetized rats resulted in severe respiratory depression and death. With lower doses there was a decrease in all parameters studied without ensuing death. Respiratory depression was even more pronounced in pentobarbitone-anesthetized rats, occurring with much lower doses of the peptide than in the urethane-anesthetized animals. beta-endorphin in the dose of 0.6 micrograms/rat still reduced respiratory frequency as well as heart rate without affecting blood pressure. Naloxone pretreatment antagonized the respiratory depression and death, while the decrease in heart rate was diminished. In conscious rats 10 microgram/rat, i.c.v., of beta-endorphin resulted in a decrease in heart rate and blood pressure without affecting respiratory frequency. It is concluded that beta-endorphin, or related opioid peptides, may be involved in cardiovascular and respiratory regulation. The effects of beta-endorphin, however, are markedly modified by the anesthetic agent used.

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