Which combination of pathways contributes to the observed increase in blood pressure from PRR overexpression?

The correct answer is that both the angiotensin II-dependent pathway and the angiotensin II-independent pathway can coexist and influence blood pressure.

Overexpression of the prorenin receptor (PRR) can lead to increased activity of the renin-angiotensin system (RAS), which primarily involves the formation of angiotensin II. This peptide hormone is well-known for its role in vasoconstriction, increasing vascular resistance, and subsequently raising blood pressure. However, PRR does not function solely through the classical angiotensin II pathway. It can also activate non-canonical pathways that contribute to blood pressure regulation.

These alternative pathways may include mechanisms such as increased sodium reabsorption in the kidneys, enhanced sympathetic nervous system activity, and other vascular responses. This dual capability means that the effects of PRR overexpression can increase blood pressure by both promoting the production of angiotensin II and facilitating additional regulatory processes independent of angiotensin II.

Therefore, acknowledging that both pathways can contribute simultaneously provides a more comprehensive understanding of how PRR overexpression influences blood pressure, highlighting the complex interplay between different hormonal systems and their effects on cardiovascular dynamics.