Increased Coronary Vascular Resistance in Spontaneously Hypertensive Rats

Klepzig, M; Eisenlohr, H; Steindl, Johannes; Strauer, B. E.

doi:10.1159/000411585

Cited by 5 publications

(2 citation statements)

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“…Regarding conductance of the coronary artery it is likely that it represents a structural adaptation of the vessels to the increased flow due to the higher metabolic requirements of the hypertensive heart. However, our results are in contrast to observations made with the same technique in coronary resistance arteries of SHRs and WKY rats (Klepzig et al, 1985). A 22-30% reduction in the diameter of SHR arteries was reported in this study, which can probably be explained by a more distal dissection site of the preparations.…”

Section: Acetylcholine Concentration (Pm1contrasting

confidence: 99%

Endothelial and smooth muscle properties of coronary and mesenteric resistance arteries in spontaneously hypertensive rats compared to WKY rats

Pourageaud

Freslon

1995

Fundamemntal Clinical Pharma

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To investigate if the functional alterations observed in resistance arteries of spontaneously hypertensive rats (SHRs) were also present at the coronary level, in vitro experiments were performed in mesenteric resistance arteries (MRA) and in right (RIC) and left interventricular coronary (LIC) arteries taken from 15-25-week-old SHR and age-matched Wistar Kyoto rats WKYs. Using a passive extension protocol, internal diameters corresponding to 100 mmHg intraluminal pressure (D100) were determined and vessels were set up to a normalized internal diameter (0.9 D100). SHR mesenteric resistance arteries had a significantly smaller diameter compared to WKY arteries, whereas both types of SHR coronary arteries had a greater diameter compared to those of WKY rats. In arteries in the absence of contracting agonist, nitro-L-arginine (NOLA, 100 microM) induced a progressive rise in basal tone, which could be reversed by subsequent addition of L-arginine (100 microM) but not D-arginine (100 microM). When expressed as percent of maximal contractions induced by agonists (noradrenaline, NA [10 microM] in MRA; serotonin, 5-HT [10 microM], in RIC and LIC), these contractions were significantly stronger in WKY compared to SHR coronary and mesenteric resistance arteries. In NA-precontracted MRA and 5HT-precontracted coronary arteries in the presence of indomethacin (10 microM), the magnitude of acetylcholine-induced maximal relaxations (expressed as percent of maximal contractions induced by agonists) was greater in WKY compared to SHR arteries. After a 30-min incubation period, NOLA (100 microM) completely inhibited relaxations induced by acetylcholine (0.01-10 microM) in all types of precontracted arteries.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Acetylcholine Concentration (Pm1contrasting

confidence: 99%

Endothelial and smooth muscle properties of coronary and mesenteric resistance arteries in spontaneously hypertensive rats compared to WKY rats

Pourageaud

Freslon

1995

Fundamemntal Clinical Pharma

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“…But there are discrepancies between different reports concerning the diameter of the coronary artery of SHR compared with that of control rats. Klepzig, Eisenlohr, Steindl & Strauer (1985) observed a 22-30% reduction in the coronary artery diameter in SHR. They dissected the arteries more distally than we did.…”

Section: Discussionmentioning

confidence: 88%

Long‐term administration of L‐arginine did not influence blood pressure, heart rate, cardiac hypertrophy or arterial wall thickness of spontaneously hypertensive rats

Kristek

1998

Experimental Physiology

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SUMMARYThe aim of this study was to evaluate whether long-term administration of L-arginine, a physiological substrate for the production of nitric oxide, improved blood pressure, heart rate, cardiac hypertrophy and particularly structural changes in the coronary and carotid artery of spontaneously hypertensive rats (SHR). The experiments started with three groups of 10-week-old animals: control Wistar rats, untreated SHR and SHR treated with L-arginine (SHR + L-arginine). L-Arginine was administered to SHR in a daily dose of 300 mg kg-1 intraperitoneally for 6 weeks. Blood pressure and heart rate were recorded each week. At the end of the experiment in one-half of each group heart weight and body weight were determined and the heart weight/body weight index was calculated. In the other animals, the cardiovascular system was perfused via the left ventricle with a glutaraldehyde fixative at 120 mmHg and the coronary and carotid arteries were processed for transmission electron microscopy. The inner diameter and wall thickness (tunica intima and tunica media) were measured on semithin sections. The reliability of the genetic feature in the SHR group was proved by the increased heart weight, heart weight/body weight index, wall thickness and wall thickness/inner diameter ratio of coronary and carotid arteries in comparison to the group of control Wistar rats. Long-term administration of L-arginine did not significantly influence blood pressure and heart rate in comparison with untreated SHR. Neither were any differences found in cardiac hypertrophy or the geometry of the coronary and carotid arteries (thickness of arterial wall, inner diameter, wall/diameter ratio). In conclusion, the changes in the cardiovascular system in SHR were not reversed, or even alleviated, by chronic treatment with L-arginine.

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