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Assessment of Vascular Tone Responsiveness using Isolated Mesenteric Arteries with a Focus on Modulation by Perivascular Adipose Tissues

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Aortic endothelial junctions in developing hypertension.

P G McGuire, T A Twietmeyer

Hypertension (Dallas, Tex. : 1979)

|July 1, 1985

Summary

This summary is machine-generated.

Hypertension alters aortic endothelial cell junctions in spontaneously hypertensive rats (SHR) even before blood pressure rises, suggesting early genetic or humoral influences on vascular adaptation.

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Area of Science:

Cardiovascular Biology
Endothelial Cell Biology
Hypertension Research

Background:

The intercellular pathway of aortic endothelium plays a crucial role in vascular function and integrity.
Spontaneously hypertensive rats (SHR) serve as a model for studying hypertension and its vascular consequences.
Understanding endothelial cell morphology changes is key to deciphering hypertension's impact.

Purpose of the Study:

To investigate the morphological changes in the intercellular pathway of aortic endothelium in spontaneously hypertensive rats (SHR) across different stages of hypertension.
To compare the morphology of aortic endothelial cells in SHR with normotensive Wistar-Kyoto rats.
To explore potential early factors influencing endothelial cell morphology in SHR.

Main Methods:

Morphological investigation of aortic endothelium in SHR and Wistar-Kyoto rats.
Analysis of tight junctions and gap junctions in endothelial cells.
Correlation of morphological findings with arterial pressure measurements at various ages.

Main Results:

SHR exhibited increased length and complexity of tight junctions compared to Wistar-Kyoto rats at all studied ages.
These tight junction alterations were observed in young SHR before significant arterial pressure elevation.
Increased gap junction area was noted in SHR, particularly at 10 weeks, coinciding with rapid blood pressure rise and increased tight junction length.

Conclusions:

Aortic endothelium in SHR shows early morphological adaptations in tight and gap junctions.
These changes suggest that factors beyond elevated blood pressure, possibly genetic or humoral, influence endothelial morphology in SHR.
The findings indicate that aortic endothelium can anticipate and partially adapt to the abnormal influences of elevated arterial pressure.