From the Guidelines

Natriuretic Peptide (NP) levels increase in hypotension.

The provided evidence does not directly address the relationship between natriuretic peptide levels and hypotension, but it does discuss the role of natriuretic peptides in heart failure and their response to various cardiac conditions.
According to the pathophysiology of natriuretic peptides, they are released in response to increased ventricular wall tension, which can occur in conditions such as heart failure, pulmonary embolism, and sepsis 1.
While the evidence does not specifically mention hypotension, it can be inferred that any condition that increases ventricular wall tension, including hypotension, may lead to an increase in natriuretic peptide levels.
However, it is essential to consider that natriuretic peptide levels can be influenced by various factors, including age, sex, and comorbidities, and their interpretation should be done cautiously 1.
In the context of heart failure, natriuretic peptide levels have been shown to parallel the clinical severity of the disease and can be used to assess prognosis and guide therapy 1.
Serial measurements of natriuretic peptide levels can also be used to track changes in risk profiles and clinical status among patients with heart failure 1.

Natriuretic peptides are released in response to increased ventricular wall tension.
Conditions that increase ventricular wall tension, such as heart failure and pulmonary embolism, can lead to an increase in natriuretic peptide levels.
Natriuretic peptide levels can be influenced by various factors, including age, sex, and comorbidities.
Serial measurements of natriuretic peptide levels can be used to track changes in risk profiles and clinical status among patients with heart failure.
The interpretation of natriuretic peptide levels should be done cautiously, considering the clinical context and potential influencing factors.

From the Research

Natriuretic peptides, including atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP), are released in response to atrial and ventricular stretch, respectively, and cause vasorelaxation, inhibition of aldosterone secretion, and inhibition of renin secretion in the kidney 2.
ANP, acting through natriuretic peptide receptor 1 (NPR1), provokes hypotension, which is thought to be due to ANP inducing vasodilation via NPR1 in the vasculature 3.
The physiologic effects of C-type natriuretic peptide (CNP) are different from those of ANP and BNP, with CNP having a hypotensive effect but no significant diuretic or natriuretic actions 2.

Controlled hypotension decreases the release of natriuretic peptides in cardiovascular healthy patients, which may be contributed to by changes in cardiac filling pressure due to lower systemic resistance and diminished perfusion pressure 4.
In patients undergoing endonasal sinus surgery, controlled hypotension using esmolol or sodium nitroprusside resulted in significantly lower concentrations of atrial and brain natriuretic peptide compared to controls 4.
However, in certain disease states, such as congestive heart failure (CHF), systemic hypertension, and acute myocardial infarction, increased blood levels of natriuretic peptides have been found, suggesting a role in the pathophysiology of those diseases 2, 5.

The natriuretic peptides have been used in the treatment of disease, with the most experience with intravenous BNP in the treatment of CHF 2.
Another pharmacologic approach being used is the inhibition of natriuretic peptide metabolism by neutral endopeptidase (NEP) inhibitor drugs, which are currently being investigated as treatments for CHF and systemic hypertension 2.
Reversible pegylation of ANP has been shown to prolong the hypotensive effect of ANP, making it a potential candidate for development into an antihypertensive drug 6.