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Altered vascular responses to circulating angiotensin II in familial combined hyperlipidemia
Gun Jörneskog1, Thomas Kahan, Mikael Ekholm
1Karolinska Institutet, Department of Clinical Sciences, Division of Medicine, Sweden, Stockholm, Sweden. gun.jorneskog@ds.se
Insights
Familial combined hyperlipidemia (FCHL) patients show impaired microvascular responses to angiotensin II, leading to increased blood pressure. This reduced vascular function may contribute to cardiovascular complications in FCHL.
Area of Science:
- Cardiovascular Physiology
- Endocrinology
- Vascular Biology
Background:
- Familial combined hyperlipidemia (FCHL) is linked to higher risks of hypertension and cardiovascular disease.
- The renin-angiotensin-aldosterone system, particularly angiotensin II, plays a key role in blood pressure regulation and vascular function.
Purpose of the Study:
- To investigate the microvascular and macrovascular responses to angiotensin II in patients with FCHL compared to healthy controls.
- To determine if FCHL affects the body's reaction to angiotensin II, a critical hormone in blood pressure control.
Main Methods:
- Sixteen FCHL patients and 16 controls received a 3-hour intravenous infusion of angiotensin II.
- Forearm skin microcirculation was assessed using laser Doppler fluxmetry to measure microvascular hyperemia at rest and during local heating.
Main Results:
- Patients with FCHL exhibited a significantly greater increase in systolic blood pressure in response to angiotensin II compared to controls.
- While controls showed enhanced microvascular hyperemia after angiotensin II infusion, FCHL patients displayed no significant change.
- Baseline systolic blood pressures were similar between the FCHL group and controls.
Conclusions:
- Angiotensin II infusion enhances microvascular hyperemia in healthy individuals but not in FCHL patients.
- Impaired microvascular dilatation capacity in FCHL may contribute to elevated blood pressure and increase the risk of cardiovascular complications.
Objectives:
Patients with familial combined hyperlipidemia (FCHL) are at increased risk of hypertension and cardiovascular disease. We examined if patients with FCHL have altered microvascular and macrovascular responses to angiotensin II, a principal mediator of the renin-angiotensin-aldosterone system.
Methods:
Sixteen patients with FCHL and 16 healthy controls were investigated before, during and after a 3 h intravenous infusion of angiotensin II (10 ng/kg/min). Forearm skin microcirculation was studied by laser Doppler fluxmetry during rest and local heating to 44 degrees C (microvascular hyperemia).
Results:
Baseline systolic blood pressures were 129 +/- 13 and 123 +/- 12 mmHg in FCHL patients and controls (P = 0.11), respectively. Angiotensin II elicited a greater systolic blood pressure response in the FCHL group (+32 +/- 13 mmHg) than in the control group (+20 +/- 11 mmHg; P < 0.001). At 3 h angiotensin II infusion, microvascular hyperemia increased in the controls (P < 0.001), whereas microvascular hyperemia was unchanged in the FCHL patients (P < 0.01, between groups).
Conclusion:
In healthy individuals, a 3 h intravenous infusion of angiotensin II enhances heat-induced microvascular hyperemia. In FCHL, this microvascular hyperemia is impaired and the systolic blood pressure response is increased. A reduced microvascular dilatation capacity in FCHL may contribute to the observed blood pressure elevation and promote development of micro- and macrovascular complications.
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