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Femoral arterial diameter and pressure were measured in anesthetized dogs. Immediately after section of the ipsilateral lumbar sympathetic chain the artery dilated, reaching a maximum of 122.0% (±0.56 SEM) of resting diameter within 30 to 40 seconds. Later the diameter diminished, stabilizing at 104.3% (±1.8 SEM) of resting diameter within 15 minutes. Stimulation of the peripheral stump of the sympathetic chain induced frequency-dependent constriction, the frequency-response curve being hyperbolic. The average maximal response was 13.42% (± 1.19 SEM) of the resting diameter. These changes were not dependent on suprarenal secretion, blood flow, or changes in distal vascular bed resistance. The contraction of the artery was slow. The half-time of stabilized contraction was 21.6 seconds at a stimulus frequency of 1/sec and 36.8 seconds at 25/sec. The half-time of relaxation was shorter (10.7 seconds and 21.5 seconds, respectively) and also frequency-dependent. A significant dilatation, after stimulation, inversely proportional to the stimulation frequency, occurred after low-frequency stimulations. The time course of contraction suggests the activation of individual smooth muscle layers successively more remote to the nerve endings, possibly due to diffusion of transmitter liberated at the nerve endings by stimulation.From the Department of Cardiovascular Physiology, Institute of Normal and Pathological Physiology, Slovak Academy of Sciences, Bratislava..

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This paper describes the myoendothelial relations in ramus interventricularis anterior and its branches in the dog and rabbit. Endothelial cells (ECs) are separated from smooth muscle cells (SMs) by fenestrated internal elastic lamina (IEL). The number of fenestrations increases towards the periphery; the first- and second-order branches have only patches of elastin in some places. ECs and SMs emit protrusions of various shapes into the fenestrae. The distance between EC and SM protrusions varies. Close appositions were also found. The diffusion of autacoids, or transmitters, as well as the electrical and biochemical mechanism of transmission seem to be involved in the transfer of information from ECs to SMs and vice versa. Biomechanical transfer (for example shear stress), via EC-SM junctions is also considered.

The diameter of a major coronary artery, the ramus interventricularis ventralis (RIV), was measured in dogs with arrested hearts perfused by an extracorporeal circulation. The resting diastolic diameter was 1.78 +/- 0.07 mm (mean +/- SE) at a diastolic pressure of 74.2 +/- 3.4 mm Hg. Bilateral supramaximal stimulation of fibers leaving the cranial pole of the stellate ganglion decreased the diameter by 71.2 +/- 8.9 micrometer, i.e., 4.0 +/- 0.5% of the resting diameter. Stimulation of the left stellate ganglion contributed 59.8 +/- 5.7% of the maximum response; that of the right contributed 40.3 +/- 5.5%. Stimulation of the thoracic ganglia (T2-4) resulted in a 1.2 +/- 0.4% decrease in coronary vessel diameter. RIV failed to respond to bilateral caudal cervical ganglion stimulation. After iv administration of phentolamine, 1-2 mg/kg, no response to sympathetic stimulation could be elicited. Therefore, it appears that alpha-receptors are activated by the release of the sympathetic neurotransmitter to sympathetic stimulation and that beta-receptors are not involved in the response of RIV to sympathetic stimulation.

In anesthetized dogs the peripheral ends of the cut sympathetic chains (LGi-LG 2 level) were stimulated while blood pressure was held constant artificially, and the diameter of the abdominal aorta was monitored. Bilateral stimulation induced a reduction in diameter that was directly related to the stimulation frequency. Maximal diameter reduction of the aorta above the iliac bifurcation averaged 8.01 ± 0.74* of resting diameter. The half-time of contraction (36.5 ±2.1 to 51.5 ± 3 . 6 seconds) was indirectly related to the stimulation frequency. The effects of right or left sympathetic chain stimulation were quantitatively similar to each other (51.3 ± 4.4% and 46.7 ± 4.5%, respectively), and the response to bilateral stimulation (92.8 ±6.1&) did not differ from the calculated value for paired unilateral stimulation (100%). A significant proximo-distal gradient of response (below the branching off of the renal arteries 2.97 ± 0.28%, at the midpoint 5.15 ± 0.52%, and above the iliac bifurcation 8.56 ± 0.79% of resting diameter) along the abdominal aorta was established during bilateral stimulation. Histochemical examination showed no corresponding differences in the density or the distribution of monoaminergic terminals. Dose-response relations for spiral strips taken from analogous aortic segments, however, displayed sensitivity to norepinephrine in the same order as the gradient in the in vivo experiments.diameter. Particularly, the range of sympathetic control of the diameter of the aorta was investigated and the functional peculiarities of the bilateral innervation were examined. In addition, the response to sympathetic stimulation along the abdominal aorta was monitored. Finally, to explain the established differences in responsiveness, both pharmacological experiments and histochemical studies were performed. MethodsExperiments were performed on 32 adult mongrel dogs of either sex weighing 11.0-19.0 kg. The dogs were anesthetized with sodium thiopental (10-15 mg/kg, iv) at the beginning of the experiment, and supplementary doses (4-7 mg/kg) were given hourly.To minimize blood losses all surgery was performed with electrocautery. After opening the abdomen with a midline incision from the xiphoid process down to the symphysis, the intestines were drawn to the left side and covered with warmed wet cotton.In 16 dogs the aorta was left intact and normally tethered except at the site where diameter was registered; at this site it was freed for a distance not longer than 5 mm. In all dogs the diameter was recorded 15-20 mm above the iliac bifurcation closely distal to the origin of the caudal mesenteric artery; the cross section of the aorta is circular at this point. In 6 dogs diameter and pressure were monitored at three sites, Site 1 was 15-20 mm above the iliac bifurcation,

The objective of the present study was to investigate the structure of the arterial walls of the offspring stemming from nitric oxide (NO)-defective hypertensive parents. The parents were treated with N Gnitro-L-arginine methyl ester (40 mg kg -1 day -1 ) for 5 weeks. Blood pressure was measured noninvasively in six 30-day-old rats and nine age-matched controls. The cardiovascular system was perfused with glutaraldehyde at 120 mmHg. The thoracic aorta and carotid artery were processed for electron microscopy, and geometry was determined by light microscopy. Endothelial cells, smooth muscle cells (SMC) and extracellular matrix (ECM) were determined by the point counting method in electron micrographs of the carotid artery. The blood pressure of experimental offspring was 150.0 ± 2.3 vs 104.6 ± 2.1 mmHg (P < 0.01) for the controls and their heart/body weight ratio of 3.9 ± 0.1 vs 4.4 ± 0.2 (P < 0.05) for the controls indicated cardiac hypotrophy. The wall thickness (tunica intima and media) of the thoracic aorta and carotid artery of experimental offspring was decreased to 78.9% (P < 0.01) and 83.8% (P < 0.01), respectively, compared to controls, as confirmed by a respective cross-sectional area of 85.3% (P < 0.01) and 84.1% (P < 0.01). The wall thickness/ inner diameter ratio was reduced to 75% (P < 0.01) in the thoracic artery and to 81.5% (P < 0.01) in the carotid artery. No change in endothelial cell volume density or ECM was observed in the tunica intima of the carotid artery, and SMC volume density was lower in the tunica media (37.6 ± 0.9 vs 44.7 ± 1.1% for controls, P < 0.01), indicating compromised SMC development. Interference with arginine metabolism, a decrease in NO, and other factors are possible mechanisms underlying the structural alterations of the cardiovascular system of offspring from NO-defective hypertensive rats.

Discrepancy was found between enhanced hypotension and attenuated relaxation of conduit arteries in response to acetylcholine (ACh) and bradykinin (BK) in nitric oxide (NO)-deficient hypertension. The question is whether a similar phenomenon occurs in spontaneously hypertensive rats (SHR) with a different pathogenesis. Wistar rats, SHR, and SHR treated with NO donors [molsidomine (50 mg/kg) or pentaerythritol tetranitrate (100 mg/kg), twice a day, by gavage] were studied. After 6 weeks of treatment systolic blood pressure (BP) was increased significantly in experimental groups. Under anesthesia, the carotid artery was cannulated for BP recording and the jugular vein for drug administration. The iliac artery was used for in vitro studies and determination of geometry. Compared to control, SHR showed a significantly enhanced (P < 0.01) hypotensive response to ACh (1 and 10 µg, 87.9 ± 6.9 and 108.1 ± 5.1 vs 35.9 ± 4.7 and 64.0 ± 3.3 mmHg), and BK (100 µg, 106.7 ± 8.3 vs 53.3 ± 5.2 mmHg). SHR receiving NO donors yielded similar results. In contrast, maximum relaxation of the iliac artery in response to ACh was attenuated in SHR (12.1 ± 3.6 vs 74.2 ± 8.6% in controls, P < 0.01). Iliac artery inner diameter also increased (680 ± 46 vs 828 ± 28 µm in controls, P < 0.01). Wall thickness, wall crosssection area, wall thickness/inner diameter ratio increased significantly (P < 0.01). No differences were found in this respect among SHR and SHR treated with NO donors. These findings demonstrated enhanced hypotension and attenuated relaxation of the conduit artery in response to NO activators in SHR and in SHR treated with NO donors, a response similar to that found in NOdeficient hypertension.