Biomedical subjects

M H Thorstad

Publications and source records attributed to M H Thorstad.

2 recordsLinked to original sources

PubMed1991

Central administration of a specific angiotensin II receptor antagonist on baroreflex function in spontaneously hypertensive rats.

To determine whether the increase in baroreflex sensitivity previously reported in lifetime captopril-treated spontaneously hypertensive rats (SHR) was due to an inhibition of brain angiotensin II mechanisms, we tested the effect of intracerebroventricular administration of an angiotensin II receptor antagonist on baroreflex control of heart rate in lifetime captopril-treated and untreated male and female SHR. Baroreceptor reflex control of heart rate was assessed by the slope of the relationship between changes in mean arterial pressure (delta MAP, mmHg) and changes in pulse interval (delta PI, ms). MAP was raised and lowered with infusions of phenylephrine and nitroprusside, respectively. Following basal assessment of baroreflex control of heart rate, rats received an intracerebroventricular injection (100 pmol) of Sar1Thr8 angiotensin II (sarthran) and reflex control of heart rate was reassessed. Adequacy of blockade was tested with central and peripheral administration of angiotensin II. Captopril-treated male (130 +/- 7 mmHg) and female (123 +/- 4 mmHg) rats had significantly lower MAP than untreated rats (174 +/- 4 and 173 +/- 8 mmHg, respectively) and enhanced bradycardia in response to increases in MAP. Intracerebroventricular administration of sarthran had no effect on basal blood pressure or heart rate but enhanced the bradycardia in response to increases in MAP in both untreated and captopril-treated rats. The increase in the slope of the line relating delta MAP to delta PT was greater for untreated than captopril-treated SHR (male untreated 2.7-fold versus captopril-treated 1.5-fold; female untreated 1.6-fold versus captopril-treated 1.5-fold).(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗

PubMed1991

Trochlear unit activity during ocular convergence.

1. Ocular convergence is usually accompanied by excyclotorsion of the eyes. Furthermore, the magnitude of cyclotorsion is dependent on the elevation of the eyes. The reason for this excyclotorsion during convergence is not understood. 2. Excyclotorsion could be produced by either increased activity in the inferior oblique muscle or decreased activity in the superior oblique muscle. An earlier study indicated that convergence may also be accompanied by a temporal (lateral) translation of the eye. This observation is more consistent with a relaxation of the superior oblique than contraction of the inferior oblique. 3. This hypothesis was tested by recording the activity of 31 neurons in the trochlear nucleus, which contains the superior oblique motoneurons. This was done in alert monkeys that were trained to make both versional and vergence eye movements. In addition, the cyclotorsion associated with convergence was measured in one of these monkeys. 4. A consistent excyclotorsion associated with convergence was observed. Trochlear unit activity decreased during convergence in all cells tested. The magnitude of this decrease was significantly greater than that seen with conjugate adduction. Furthermore, the size of the decrease varied systematically with ocular elevation in a manner that was consistent with earlier measures of cyclotorsion during convergence. 5. These results suggest that the excyclotorsion seen during convergence, and perhaps the lateral translation of the eye, are due to a relaxation of the superior oblique muscle. This relaxation during convergence is greater than that which accompanies similar conjugate movements of the eyes. We hypothesize that this peculiar pattern of muscle innervation has a motor rather than sensory function.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗