Myoedothelial connection, a relationship between spiral arrangement of smooth muscle cells and endothelium in resistance muscular arteries

Conventionally, the architecture of the artery wall is based upon the close-packed smooth muscle cells, endothelial and adventitial cells in both sides of internal elastic lamina [IEL]. However, the adventitia and endothelium are now viewed as key players in vascular growth and repair. Recent work raises fundamental questions about the cellular heterogeneity of arteries, time course, triggering of normal and pathological re-modeling. Twelve wild type mice were employed. After killing with CO2 inhalation, dissected mesenteric arteries were removed and cleaned with adipose tissue. Arteries were mounted in the perfusion pressure myograph under normal pressure [70mmHg] in Kreb's solution, which bubbled with 95% O2 and 5% CO2 to pH 7.4, at 37 C. After staining with fluorescent ligands [Syto 13] for nuclei and [DIO 1mM] for cytoplasm, arteries were scanned with the Laser Scanning Co focal Microscopy [LSCM] under [488nm/515nm], [484nm/501nm] and [543nm/580nm] Argon-Helium ion laser wavelength. Three dimensional images of computer observation suggest that there may be a close relationship between the helical organization of smooth muscle cells and the underlying pattern of endothelial cells [myoendothelial connection]. Tight junctions between cells must be broken and remade during the remodeling process. This suggests a carefully controlled defensive structure for intra-cellular connections, that is capable of withstanding the acute stresses of normal function, but which must be capable of modification to adapt to a new state, when the bio-physical conditions dictate. Endothelial mosaicism related to spiral arrangements of underlying smooth muscle cells, are associated with the functional cell connections. Taken together, these issues provide an exciting new phase in understanding the physiological modeling of the vascular wall, producing a new view of the dynamic nature of vascular structure

Potentiation of responses to UK-14304 in rat isolated common carotid artery by angiotensin

The selective [alpha 2] -adrenoceptor agonist UK-14304 produces a small vasoconstrictor response in the rat isolated carotid artery. The purpose of the work presented here was to investigate whether stimuli that produce submaximal contraction would potentiate responses to UK-14304. Male Wistar rats were killed by overdose with pentobarbitone sodium, after which the left and right common carotid arteries were removed. The rings of arteries 3-4 mm in length were cut from each vessel and then mounted in 10 mL isolated organ bath, bathed in Krebs maintained at 37°C and gassed with 95% 02 plus 5% CO[2] The preparations were allowed to equilibrate for an hour. Cumulative concentration-response curves [CCRC] were constructed in a cumulative manner by increasing the concentration of the agonists in half-log increments. When antagonists were used, the preparations were incubated at least for 45 minutes with the drugs prior to the onset of a second CCRC. Angiotensin II [All] and other contracting factors were added approximately 10-15 min prior to the onset of CCRC to an agonist. After inducing tone with low concentrations of the thromboxane A[2] mimetic agent U-46619 [1nM], 5HT [0.5-1 [micro] M] and phenylephrine [10 [micro] M], exposure of the preparation to UK-14304 resulted in concentration dependent contractions to this agonist. The sensitivity and maximum response of the preparation to UK-14304 were not changed. Inducing tone with AII [0.01 [micro] M] produced a significant leftward shift in the CCRC to UK-14304 [p<0.05]. Thus submaximal contraction with AII [0.01 [micro] M],increased responses significantly, but inducing tone with phenylephrine, U-46619 and 5HT had no effect on responses to UK-14304. The [alpha] -adrenoceptor antagonists prazosin and rauwolscine were examined to see whether UK-14304's main action in the presence of All remained via [alpha 1]. The potentiated responses were prazosin sensitive and rauwolscine resistant, indicating an increasing effect mediated by [alpha 1] -adrenoceptotrs