Table 2 Causative factors for changes in vascular structure
Mechanism | Evidence | References |
|---|---|---|
Sympathetic nervous system |  Sympathetic activity increased in large proportion of human hypertensive patients | |
|  |  Tachycardia present in pre-hypertensive SHR was good predictor of eventual BP outcome | |
|  |  Higher innervation density in cerebral arteries of SHR vs. WKY 1 day after birth | |
|  |  Higher innervation density in mesenteric arteries of SHR vs. WKY 10 days after birth | |
|  |  Neonatal sympthectomy prevented hypertension development and structural/functional changes in mesenteric arteries of SHR | |
|  |  Neonatal treatment with capsaicin prevented hypertension in SHR | |
Renin–angiotensin System |  Ang II infusion induced hypertension development and increased medial area of mesenteric vessels | |
|  |  Ang II infusion caused changes in mesenteric artery and aorta PVAT function | |
|  |  Ang II infusion caused structural and functional changes in mesenteric arteries that are associated with hypertension development and cardiac hypertrophy | |
|  |  ACE inhibitor treatment of SHR before and after birth prevented hypertension development and cardiac hypertrophy | |
|  |  ACE inhibitor treatment in SHR prevented medial wall hypertrophy and an increase in SMC layers in mesenteric arteries through induction of SMC apoptosis | |
|  |  AT1 receptor antagonist treatment lowered BP and decreased wall thickness in mesenteric arteries but did not lower BP permanently | |
|  |  ACE inhibitor treatment caused production of Ang-(1–7) and accumulation of bradykinin | |
|  |  Infusion of Ang-(1–7) lowered BP in SHR | |
|  |  Treatment with epalapril in young SHR prevents further development of vascular hypertrophy of renal vessels | |
|  |  Treatment of enalapril in adult SHR reversed vascular hypertrophy in mesenteric arteries and some large renal vessels | |
DNA synthesis/apoptosis |  Newborn SHR superior and large mesenteric arteries are similar to WKY suggesting structural changes occur after birth through differentiation of myofibroblasts or proliferation of SMC | |
|  |  Autoradiographic studies show higher large mesenteric artery SMC labeling in SHR than WKY after 1 week post birth, but similar in older age groups | |
|  |  At 6 weeks when SHR BP becomes higher than WKY, higher labeling in SHR SMC found in aorta, renal artery, femoral artery | |
|  |  1–2 week SHR have lower incidence of apoptotic SMC than WKY |